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Degos, Vincent, Tifenn Le charpentier, Vibol Chhor, Olivier Brissaud, Sophie Lebon, Leslie Schwendimann, Nathalie Bednareck, Sandrine Passemard, Jean Mantz, and Pierre Gressens. "Neuroprotective Effects of Dexmedetomidine against Glutamate Agonist-induced Neuronal Cell Death Are Related to Increased Astrocyte Brain-derived Neurotrophic Factor Expression." Anesthesiology 118, no. 5 (May 1, 2013): 1123–32. http://dx.doi.org/10.1097/aln.0b013e318286cf36.
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Abstract Background: Brain-derived neurotrophic factor (BDNF) plays a prominent role in neuroprotection against perinatal brain injury. Dexmedetomidine, a selective agonist of α2-adrenergic receptors, also provides neuroprotection against glutamate-induced damage. Because adrenergic receptor agonists can modulate BDNF expression, our goal was to examine whether dexmedetomidine’s neuroprotective effects are mediated by BDNF modulation in mouse perinatal brain injury. Methods: The protective effects against glutamate-induced injury of BDNF and dexmedetomidine alone or in combination with either a neutralizing BDNF antibody or an inhibitor of the extracellular signal-regulated kinase pathway (PD098059) were compared in perinatal ibotenate-induced cortical lesions (n = 10–20 pups/groups) and in mouse neuronal cultures (300 μm of ibotenate for 6 h). The effect of dexmedetomidine on BDNF expression was examined in vivo and in vitro with cortical neuronal and astrocyte isolated cultures. Results: Both BDNF and dexmedetomidine produced a significant neuroprotective effect in vivo and in vitro. Dexmedetomidine enhanced Bdnf4 and Bdnf5 transcription and BDNF protein cortical expression in vivo. Dexmedetomidine also enhanced Bdnf4 and Bdnf5 transcription and increased BDNF media concentration in isolated astrocyte cultures but not in neuronal cultures. Dexmedetomidine’s protective effect was inhibited with BDNF antibody (mean lesion size ± SD: 577 ± 148 μm vs. 1028 ± 213 μm, n = 14–20, P < 0.001) and PD098059 in vivo but not in isolated neuron cultures. Finally, PD098059 inhibited the increased release of BDNF induced by dexmedetomidine in astrocyte cultures. Conclusion: These results suggest that dexmedetomidine increased astrocyte expression of BDNF through an extracellular signal-regulated kinase-dependent pathway, inducing subsequent neuroprotective effects.
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Ding, Baojin, Paul R. Dobner, Debra Mullikin-Kilpatrick, Wei Wang, Hong Zhu, Chi-Wing Chow, John W. Cave, Richard M. Gronostajski, and Daniel L. Kilpatrick. "BDNF activates an NFI-dependent neurodevelopmental timing program by sequestering NFATc4." Molecular Biology of the Cell 29, no. 8 (April 15, 2018): 975–87. http://dx.doi.org/10.1091/mbc.e16-08-0595.
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How intrinsic and extrinsic signals are coordinated to regulate synaptic maturation and its timing is an important question for neurodevelopment and its disorders. We investigated the influence of the neurotrophin BDNF on the developmental timing of a dendrite/synapse-related gene program controlled by nuclear factor I (NFI) in maturing cerebellar granule neurons (CGNs). BDNF accelerated the onset of NFI-regulated late-gene expression and NFI temporal occupancy in CGN cultures in a MEK5/ERK5-dependent manner. BDNF and NFI occupancy were mutually regulating, with BDNF enhancing the temporal binding of NFI to the Bdnf4 promoter itself. Moreover, BDNF induced phosphorylation and accelerated the departure of the trans-repressor NFATc4 from NFI late-gene promoters, including Bdnf4, which is permissive for NFI binding. BDNF dismissal of NFATc4 from late genes was linked to MEK5/ERK5-dependent sequestration of NFATc4 in the cis–Golgi, an event mirrored in CGNs developing in vivo. These studies reveal an expanded autoregulatory gene network for NFI temporal occupancy involving BDNF and NFATc4 extranuclear sequestration. Based on these and earlier findings, NFATc4 integrates intrinsic developmental signaling from membrane potential/calcineurin and autocrine/paracrine BDNF/TrkB to control initiation of NFI occupancy in maturing CGNs. We also identify a local Bdnf/Etv1 gene circuit within the larger NFI autoregulatory network.
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Efffendy, Elmeida, Muhammad Sjahrir, and Nurul Utami. "The Relationship between Brain-derived Neurotrophic Factor’s Serum Level and Hospital Anxiety and Depression Scale-depression in Patients with Psoriasis Vulgaris." Open Access Macedonian Journal of Medical Sciences 9, T3 (May 20, 2021): 164–67. http://dx.doi.org/10.3889/oamjms.2021.6290.
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BACKGROUND: Psoriasis vulgaris is a chronic inflammatory skin disorder that can lead to depression. The involvement of the nervous system in psoriasis was proved by the influence of brain-derived neurotrophic factor (BDNF) in regulating corneocyte homeostasis. Low level of BDNF in patients with psoriasis result in transit amplifying subpopulation of basal keratinocytes not performing their function as inhibitors of keratinocyte proliferation, resulting in acceleration of keratinocyte proliferation. In depressed patients, it is known that levels of BDNF in the serum and hippocampus are low. BDNF level imbalance potentially affects the severity of psoriasis and depression. METHODS: This is an analytical cross-sectional study. The measurement of BDNFs serum level was carried out in the Medan Private Laboratory using a human BDNF (R and D®, USA) kit using the ELISA method. We use hospital anxiety and depression scale (HADS-D) questionnaire to assess depression symptoms. RESULTS: The results of the Spearman correlation test for BDNFs serum level and HADS-D showed p < 0.05, it can be concluded that there is a correlation between BDNFs serum level and HADS-D. The strength of the relationship between HADS-D and BDNFs serum level is −0.537 that shows moderate correlation (r = 0.4 −<0.6). Relationship between HADS-D and BDNFs serum level is −0.537 that shows moderate correlation (r = 0.4 −<0.6). CONCLUSION: This study shows a moderate negative relationship between BDNFs serum level and the degree of symptoms of depression, which the lower level of BDNFs serum will increase the degree of depression symptoms.
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Jo, Danbi, Yujeong Son, Gwangho Yoon, Juhyun Song, and Oh Yoen Kim. "Role of Adiponectin and Brain Derived Neurotrophic Factor in Metabolic Regulation Involved in Adiposity and Body Fat Browning." Journal of Clinical Medicine 10, no. 1 (December 26, 2020): 56. http://dx.doi.org/10.3390/jcm10010056.
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Obesity, characterized by excessive fat mass, has been emerging as a major global epidemic and contributes to the increased risk of morbidity around the world. Thus, the necessity to find effective therapy and specific regulatory mechanisms is increasing for controlling obesity. Lately, many researchers have been interested in the linkage between obesity and adipokines/myokines, particularly adiponectin and brain-derived neurotrophic factor (BDNF). However, the role of adiponectin and BDNF in adiposity has not been clearly defined yet. We examined the association of adiposity with adiponectin and BDNF through human study (observational study) with Korean women and in vitro experiments. In the human study, we found a negative relationship between adiposity and circulating adiponectins but irregular patterns in the relationship between adiposity and circulating BDNFs. In the in vitro study using 3T3-L1 adipocytes, adiponectin treatment strongly promoted adipocyte differentiation and the fat browning process, whereas BDNF treatment attenuated adipocyte differentiation and the fat browning process in differentiated adipocytes. Our results demonstrate that adiponectin and BDNF play an important role in regulating fat mass and the expression of fat-browning markers in different ways, and also suggest that circulating adiponectin may be used as an important monitoring index for obesity status.
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Baglan Yentur, S., Z. Ercan, G. Deniz, A. Karatas, M. Gur, G. Alkan, and S. S. Koca. "POS0576 EFFECTS OF ACUTE EXERCISE ON SERUM BDNF LEVEL IN PATIENTS WITH RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 522.1–522. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3768.
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Background:Brain derived neurotrophic factor (BDNF) is a neurotrofic factor that may show healing, survival-promoting and protective effects on neurons in central and peripheral nervous system. The effect of physical exercise on serum BDNF is unclear. Also, BDNF level was found significantly lower in rheumatoid Arthritis (RA) patients with depression.Objectives:Aim of this study is to investigate the variation of BDNF levels following acute exercise and potential correlation between BDNF levels and depression.Methods:This study included 44 RA patients and 44 age and sex matched healthy controls (HC). Aerobic exercise was performed to all participants for a single session. The intervention was performed on a treadmill and included 5 minutes of warm-up, 20 minutes of walking exercise reaching at 60- 80% of Maximal heart rate and 5 minutes of cool-down. Depression and anxiety levels were evaluated with Beck Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS). Blood samples from all subjects were taken and centrifuged before and immediately after the exercise intervention.Results:Serum BDNF levels (both baseline and post-exercise) were similar in the RA and HC group (Table 1). Although after aerobic exercise serum BDNF levels were significantly decreased in both RA and HC groups (Wilcoxon Rank P < 0.05) ΔBDNF levels was significantly higher in the RA group than HC group. Serum BDNF level was increased in 30.2% of healthy subjects and 4.5% of RA patients (P = 0.002). On the other hand, BDI, HADS depression and HADS anxiety indices were correlated significantly with ΔBDNF levels in the RA group (p<0.05) but not in HC group.Conclusion:A single bout of exercise may be effective on serum BDNF levels in patients with RA and healthy subjects. However, psychological comorbidities affect the amelioration of BDNF level, in RA. The long-term effect of alterations on BDF level is candidate to evaluate by prospective studies.Table 1.Clinical and laboratory characteristics in the study groupsRA (n=44)HC (n=44)PMean age, years46.8±10.343.4±6.40.071*Females, n (%)32 (72.7)31 (70.5)0.813**Active smokers, n (%)12 (27.3)10 (22.7)0.622**BMI, kg/m226.8±4.625.6±2.40.127*HADS Depression10.2±3.92.2±2.1<0.001*HADS Anxiety10.4±4.12.4±2.1<0.001*BDI17.9±8.13.7±4.1<0.001*BDNF (baseline), pg/ml798.9±381.1688.7±469.90.069***BDNF (post-exercise), pg/ml469.5±193.5509.9±380.40.593***ΔBDNF, pg/ml329.5±258.4211.1±302.60.047***BDNF increased, n (%)2 (4.5)13 (30.2)0.002**RA; rheumatoid arthritis, HC; healthy control, BMI; body mass index, HADS; Hospital Anxiety and Depression Scale, BDI; Beck Depression Inventory, BDNF; brain derived neurotrophic factor*Student’s t test, **Chi square test and ***Mann Whitney U testDisclosure of Interests:None declared
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McAllister, A. Kimberley. "BDNF." Current Biology 12, no. 9 (April 2002): R310. http://dx.doi.org/10.1016/s0960-9822(02)00825-4.
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Wong, Yu-Hui, Chia-Ming Lee, Wenjun Xie, Bianxiao Cui, and Mu-ming Poo. "Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin." Proceedings of the National Academy of Sciences 112, no. 32 (July 27, 2015): E4475—E4484. http://dx.doi.org/10.1073/pnas.1511830112.
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Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation.
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Пальцын, А. А. "Brain-derived neurotrophic factor (BDNF)." Nauchno-prakticheskii zhurnal «Patogenez», no. 3() (December 12, 2019): 83–88. http://dx.doi.org/10.25557/2310-0435.2019.03.83-88.
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Сегодня нейротрофический фактор мозга (BDNF) - вещество очень популярное. Большой интерес к белку объясняется его участием в важнейших для жизни и здоровья процессах: нервной регуляции, углеводном и липидном обмене, адаптации к физическим нагрузкам. Вещество участвует в регуляции эффективности профилактических и лечебных процедур, эмоционального состояния, стрессоустойчивости, нейропластичности, нейрогенеза. BDNF - главный регулятор действия самого универсального и, часто, самого эффективного лечебного средства - физических нагрузок. Следовательно, он становится веществом первостепенного значения в одной из самых актуальных проблем современной медицины - профилактике и лечении гипертонической болезни. Кроме гипотензивного действия, доказана эффективность BDNF при обусловленных гипертонией когнитивных нарушениях, шизофрении, дефектах памяти, эмоциональных расстройствах. Today, the brain-derived neurotrophic factor (BDNF) is a very popular substance. The high interest to this protein is due to its participation in key processes for life and health, including nervous regulation, carbohydrate and lipid metabolism, and exercise capacity. BDNF regulates preventive and therapeutic efficacy of exercise, emotional state, stress resistance, neuroplasticity, and neurogenesis. BDNF determines the action of the most universal and often the most effective therapeutic means, physical exercise. Therefore, BDNF appears to be the substance of primary importance for a burning issue of current medicine, prevention and treatment of hypertension. In addition to its hypotensive effect, BDNF has proved to be beneficial in hypertension-induced cognitive decline, schizophrenia, memory impairment, and emotional disorders.
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Chu, Pengcheng, Wei Guo, He You, and Bai Lu. "Regulation of Satiety by Bdnf-e2-Expressing Neurons through TrkB Activation in Ventromedial Hypothalamus." Biomolecules 13, no. 5 (May 11, 2023): 822. http://dx.doi.org/10.3390/biom13050822.
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The transcripts for Bdnf (brain-derived neurotrophic factor), driven by different promoters, are expressed in different brain regions to control different body functions. Specific promoter(s) that regulates energy balance remain unclear. We show that disruption of Bdnf promoters I and II but not IV and VI in mice (Bdnf-e1−/−, Bdnf-e2−/−) results in obesity. Whereas Bdnf-e1−/− exhibited impaired thermogenesis, Bdnf-e2−/− showed hyperphagia and reduced satiety before the onset of obesity. The Bdnf-e2 transcripts were primarily expressed in ventromedial hypothalamus (VMH), a nucleus known to regulate satiety. Re-expressing Bdnf-e2 transcript in VMH or chemogenetic activation of VMH neurons rescued the hyperphagia and obesity of Bdnf-e2−/− mice. Deletion of BDNF receptor TrkB in VMH neurons in wildtype mice resulted in hyperphagia and obesity, and infusion of TrkB agonistic antibody into VMH of Bdnf-e2−/− mice alleviated these phenotypes. Thus, Bdnf-e2-transcripts in VMH neurons play a key role in regulating energy intake and satiety through TrkB pathway.
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McAllan, Liam, Kristen R. Maynard, Alisha S. Kardian, Amanda S. Stayton, Shelby L. Fox, Erin J. Stephenson, Clint E. Kinney, et al. "Disruption of brain-derived neurotrophic factor production from individual promoters generates distinct body composition phenotypes in mice." American Journal of Physiology-Endocrinology and Metabolism 315, no. 6 (December 1, 2018): E1168—E1184. http://dx.doi.org/10.1152/ajpendo.00205.2018.
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Brain-derived neurotrophic factor (BDNF) is a key neuropeptide in the central regulation of energy balance. The Bdnf gene contains nine promoters, each producing specific mRNA transcripts that encode a common protein. We sought to assess the phenotypic outcomes of disrupting BDNF production from individual Bdnf promoters. Mice with an intact coding region but selective disruption of BDNF production from Bdnf promoters I, II, IV, or VI (Bdnf-e1−/−, -e2−/−, -e4−/−, and -e6−/−) were created by inserting an enhanced green fluorescent protein-STOP cassette upstream of the targeted promoter splice donor site. Body composition was measured by MRI weekly from age 4 to 22 wk. Energy expenditure was measured by indirect calorimetry at 18 wk. Food intake was measured in Bdnf-e1−/− and Bdnf-e2−/− mice, and pair feeding was conducted. Weight gain, lean mass, fat mass, and percent fat of Bdnf-e1−/− and Bdnf-e2−/− mice (both sexes) were significantly increased compared with wild-type littermates. For Bdnf-e4−/− and Bdnf-e6−/− mice, obesity was not observed with either chow or high-fat diet. Food intake was increased in Bdnf-e1−/− and Bdnf-e2−/− mice, and pair feeding prevented obesity. Mutant and wild-type littermates for each strain (both sexes) had similar total energy expenditure after adjustment for body composition. These findings suggest that the obesity phenotype observed in Bdnf-e1−/− and Bdnf-e2−/− mice is attributable to hyperphagia and not altered energy expenditure. Our findings show that disruption of BDNF from specific promoters leads to distinct body composition effects, with disruption from promoters I or II, but not IV or VI, inducing obesity.
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Gutiérrez-Vargas, Randall, Alexis Ugalde-Ramírez, Markel Rico-González, José Pino-Ortega, Juan González-Hernández, and Daniel Rojas-Valverde. "A Systematic Review of the Effects of Football Playing on Changes in Serum Brain-Derived Neurotrophic Factor Level." Applied Sciences 11, no. 24 (December 13, 2021): 11828. http://dx.doi.org/10.3390/app112411828.
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Background: Consistent evidence suggests that exercise improves cognition and decision making, with preliminary evidence suggesting that brain-derived neurotrophic factors (BDNFs) may mediate these effects on high-intensity interval activities, such as in football playing. We conducted a systematic review of studies on football players or football task interventions that evaluated the causality of exercise or its relationship with changes in the basal BDNF level. Methods: The search was conducted in PubMed, SPORTDiscus, Cochrane, and FECYT (Web of Sciences, CCC, DIIDW, KJD, MEDLINE, RSCI, and SCIELO) according to the guidelines for performing systematic reviews in the sport sciences field. Results: From the 44 studies initially identified, seven studies were fully reviewed, and their outcome measures were extracted and analysed. In the scientific study of football, the studies published thus far have explored the relationship of serum BDNF levels and other cognitive function factors with the genetic expression of polymorphisms, the anthropometric and fitness conditions, the acute exercise effect of the match, and the typical actions of the match such as heading. Conclusions: The heterogeneity of designs and variables evaluated in studies related to BDNF exercise or interaction and football playing does not allow us to conclusively determine that there is a relationship with the cause or effect of genetic, anthropometric, or conditional factors that derive from an increase in BDNF due to actions during the playing of football.
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Agosto-Marlin, Ibis M., and Gordon S. Mitchell. "Spinal BDNF-induced phrenic motor facilitation requires PKCθ activity." Journal of Neurophysiology 118, no. 5 (November 1, 2017): 2755–62. http://dx.doi.org/10.1152/jn.00945.2016.
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Spinal brain-derived neurotrophic factor (BDNF) is necessary and sufficient for certain forms of long-lasting phrenic motor facilitation (pMF). BDNF elicits pMF by binding to its high-affinity receptor, tropomyosin receptor kinase B (TrkB), on phrenic motor neurons, potentially activating multiple downstream signaling cascades. Canonical BDNF/TrkB signaling includes the 1) Ras/RAF/MEK/ERK MAP kinase, 2) phosphatidylinositol 3‐kinase (PI3K)/Akt, and 3) PLCγ/PKC pathways. Here we demonstrate that spinal BDNF-induced pMF requires PLCγ/PKCθ in normal rats but not MEK/ERK or PI3K/Akt signaling. Cervical intrathecal injections of MEK/ERK (U0126) or PI3K/Akt (PI-828; 100 μM, 12 μl) inhibitor had no effect on BDNF-induced pMF (90 min after BDNF; U0126 + BDNF: 59 ± 14%, PI-828 + BDNF: 59 ± 8%, inhibitor vehicle + BDNF: 56 ± 7%; all P ≥ 0.05). In contrast, PKCθ inhibition with theta inhibitory peptide (TIP; 0.86 mM, 12 μl) prevented BDNF-induced pMF (90 min after BDNF; TIP + BDNF: −2 ± 2%; P ≤ 0.05 vs. other groups). Thus BDNF-induced pMF requires downstream PLCγ/PKCθ signaling, contrary to initial expectations. NEW AND NOTEWORTHY We demonstrate that BDNF-induced pMF requires downstream signaling via PKCθ but not MEK/ERK or PI3K/Akt signaling. These data are essential to understand the sequence of the cellular cascade leading to BDNF-dependent phrenic motor plasticity.
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Kingwell, Katie. "BDNF copycats." Nature Reviews Drug Discovery 9, no. 6 (June 2010): 433. http://dx.doi.org/10.1038/nrd3190.
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Yates, Darran. "Locating BDNF." Nature Reviews Neuroscience 13, no. 5 (April 4, 2012): 291. http://dx.doi.org/10.1038/nrn3238.
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Mayeur, Sylvain, Marie-Amélie Lukaszewski, Christophe Breton, Laurent Storme, Claudine Junien, Didier Vieau, and Jean Lesage. "Le BDNF." médecine/sciences 27, no. 3 (March 2011): 251–52. http://dx.doi.org/10.1051/medsci/2011273251.
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Corrêa, Jôice Dias, Daniele Sirineu Pereira, Mila Fernandes Moreira Madeira, Celso Martins Queiroz-Junior, Danielle Glória Souza, Mauro Martins Teixeira, José Eustáquio Costa, Antônio Lúcio Teixeira, and Tarcília Aparecida da Silva. "Brain-Derived Neurotrophic Factor in Chronic Periodontitis." Mediators of Inflammation 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/373765.
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Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family. Outside the nervous system, BDNF has been shown to be expressed in various nonneural tissues, such as periodontal ligament, dental pulp, and odontoblasts. Although a role for BDNF in periodontal regeneration has been suggested, a function for BDNF in periodontal disease has not yet been studied. The aim of this study was to analyze the BDNF levels in periodontal tissues of patients with chronic periodontitis (CP) and periodontally healthy controls (HC). All subjects were genotyped for the rs4923463 and rs6265 BDNF polymorphisms. Periodontal tissues were collected for ELISA, myeloperoxidase (MPO), and microscopic analysis from 28 CP patients and 29 HC subjects. BDNF levels were increased in CP patients compared to HC subjects. A negative correlation was observed when analyzing concentration of BDNF and IL-10 in inflamed periodontium. No differences in frequencies of BDNF genotypes between CP and HC subjects were observed. However, BDNF genotype GG was associated with increased levels of BDNF, TNF-α, and CXCL10 in CP patients. In conclusion, BDNF seems to be associated with periodontal disease process, but the specific role of BDNF still needs to be clarified.
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Fachim, Helene A., Nagaraj Malipatil, Kirk Siddals, Rachelle Donn, Gabriela Y. Cortés, Caroline F. Dalton, J. Martin Gibson, and Adrian H. Heald. "Methylation Status of Exon IV of the Brain-Derived Neurotrophic Factor (BDNF)-Encoding Gene in Patients with Non-Diabetic Hyperglycaemia (NDH) before and after a Lifestyle Intervention." Epigenomes 6, no. 1 (February 18, 2022): 7. http://dx.doi.org/10.3390/epigenomes6010007.
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BDNF signalling in hypothalamic neuronal circuits is thought to regulate mammalian food intake. In light of this, we investigated how a lifestyle intervention influenced serum levels and DNA methylation of BDNF gene in fat tissue and buffy coat of NDH individuals. In total, 20 participants underwent anthropometric measurements/fasting blood tests and adipose tissue biopsy pre-/post-lifestyle (6 months) intervention. DNA was extracted from adipose tissue and buffy coat, bisulphite converted, and pyrosequencing was used to determine methylation levels in exon IV of the BDNF gene. RNA was extracted from buffy coat for gene expression analysis and serum BDNF levels were measured by ELISA. No differences were found in BDNF serum levels, but buffy coat mean BDNF gene methylation decreased post-intervention. There were correlations between BDNF serum levels and/or methylation and cardiometabolic markers. (i) Pre-intervention: for BDNF methylation, we found positive correlations between mean methylation in fat tissue and waist-hip ratio, and negative correlations between mean methylation in buffy coat and weight. (ii) Post-intervention: we found correlations between BDNF mean methylation in buffy coat and HbA1c, BDNF methylation in buffy coat and circulating IGFBP-2, and BDNF serum and insulin. Higher BDNF % methylation levels are known to reduce BNDF expression. The fall in buffy coat mean BDNF methylation plus the association between lower BDNF methylation (so potentially higher BDNF) and higher HbA1c and serum IGFBP-2 (as a marker of insulin sensitivity) and between lower serum BDNF and higher circulating insulin are evidence for the degree of BDNF gene methylation being implicated in insulinisation and glucose homeostasis, particularly after lifestyle change in NDH individuals.
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Machado Dias, Alvaro. "Bioinformatics Approach to BDNF and BDNF-Related Disorders." Current Neuropharmacology 9, no. 2 (June 1, 2011): 318–29. http://dx.doi.org/10.2174/157015911795596586.
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Aktener, Ahmet, Koksal Alptekin, Berna Kivircik-Akdede, Halis Ulas, A. George Awad, Ceyhun Can, Nese Cengizcetin, Seda Mertol, Meral Oguz, and Serhat Taslica. "SERUM BDNF AND mRNA BDNF LEVELS IN SCHIZOPHRENIA." Schizophrenia Research 102, no. 1-3 (June 2008): 178. http://dx.doi.org/10.1016/s0920-9964(08)70543-7.
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Стамбольский, Д. В., О. С. Плеханова, И. Ю. Юдина, Н. И. Калинина, М. Н. Карагяур, В. Э. Дубров, А. Ю. Кочиш, et al. "The brain-derived neurotrophic factor (BDNF) system as a therapeutical target for development of drugs restoring innervation." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 4(61) (December 19, 2017): 142–52. http://dx.doi.org/10.25557/igpp.2017.4.8534.
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Мозговой нейротрофический фактор (BDNF) является одним из основных нейротрофических факторов, участвующих в поддержании функционирования и регенерации нервной системы. В последние годы BDNF рассматривают как многообещающую терапевтическую мишень, на основании полученных данных о том, что BDNF улучшает регенерацию нейронов. Цель обзора - суммировать данные об экспрессии BDNF, его сигнализации, эффектах и механизмах стимуляции реиннервации. Анализ исследований последних десятилетий позволяет сделать заключение о целесообразности и перспективности разработок, направленных на создание лекарственных препаратов на основе BDNF для регенерации компонентов нервной системы. Brain-derived neurotrophic factor (BDNF) is a major neurotrophic factor maintaining the nervous system function and regeneration. Based on reports indicating that BDNF enhances neuronal regeneration, in recent years, BDNF has been considered a promising therapeutic target. The aim of this review was to summarize current data on BDNF expression, signaling, and mechanisms for stimulation of reinnervation. Conclusion. Recent studies of the role of BDNF showed that continuation of research and development of BDNF-based drugs stimulating regeneration of nervous system components is advisable and promising.
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Mudjihartini, Ninik. "Brain-derived neurotrophic factor (BDNF) dan proses penuaan: sebuah tinjauan." Jurnal Biomedika dan Kesehatan 4, no. 3 (September 30, 2021): 120–29. http://dx.doi.org/10.18051/jbiomedkes.2021.v4.120-129.
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Brain-derived neurotrophic factor (BDNF) merupakan faktor neurotrofin yang berpengaruh dalam mendukung pembentukan, perkembangan neuron, dan mempertahankan keberadaan neuron. BDNF dapat ditemukan dan aktif pada hipokampus, korteks, dan otak depan. Penuaan merupakan proses multifaktorial yang ditentukan oleh faktor genetik dan faktor epigenetik. Penurunan kadar BDNF menurunkan kemampuan belajar dan mengingat, terjadi pada orang lanjut usia atau yang mengalami penyakit neurodegeneratif. Penelitian membuktikan bahwa kadar BDNF yang tinggi mampu meningkatkan plastisitas neuron. BDNF memiliki reseptor TrkB dan p75 yang menentukan suatu neuron dapat bertahan hidup atau sebaliknya terjadi apoptosis. BDNF-TrkB mendukung pembentukan short term memory dan perkembangan neuron khususnya dendrit. BDNF-p57 mengaktifkan NFkB yang berperan dalam maturasi sistem saraf pusat. Peran BDNF sangat dipengaruhi oleh reseptornya. Nutrisi, metabolisme, perilaku, dan stres memengaruhi ekspresi BDNF. Faktor lingkungan yang meningkatkan kadar BDNF dapat menunda penuaan dan meningkatkan kemampuan kognitif.
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Lemos, José R., Cleber R. Alves, Sílvia B. C. de Souza, Julia D. C. Marsiglia, Michelle S. M. Silva, Alexandre C. Pereira, Antônio L. Teixeira, et al. "Peripheral vascular reactivity and serum BDNF responses to aerobic training are impaired by the BDNF Val66Met polymorphism." Physiological Genomics 48, no. 2 (February 2016): 116–23. http://dx.doi.org/10.1152/physiolgenomics.00086.2015.
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Besides neuronal plasticity, the neurotrophin brain-derived neurotrophic factor (BDNF) is also important in vascular function. The BDNF has been associated with angiogenesis through its specific receptor tropomyosin-related kinase B (TrkB). Additionally, Val66Met polymorphism decreases activity-induced BDNF. Since BDNF and TrkB are expressed in vascular endothelial cells and aerobic exercise training can increase serum BDNF, this study aimed to test the hypotheses: 1) Serum BDNF levels modulate peripheral blood flow; 2) The Val66Met BDNF polymorphism impairs exercise training-induced vasodilation. We genotyped 304 healthy male volunteers (Val66Val, n = 221; Val66Met, n = 83) who underwent intense aerobic exercise training on a running track three times/wk for 4 mo. We evaluated pre- and post-exercise training serum BDNF and proBDNF concentration, heart rate (HR), mean blood pressure (MBP), forearm blood flow (FBF), and forearm vascular resistance (FVR). In the pre-exercise training, BDNF, proBDNF, BDNF/proBDNF ratio, FBF, and FVR were similar between genotypes. After exercise training, functional capacity (V̇o2 peak) increased and HR decreased similarly in both groups. Val66Val, but not Val66Met, increased BDNF (interaction, P = 0.04) and BDNF/proBDNF ratio (interaction, P < 0.001). Interestingly, FBF (interaction, P = 0.04) and the FVR (interaction, P = 0.01) responses during handgrip exercise (HG) improved in Val66Val compared with Val66Met, even with similar responses of HR and MBP. There were association between BDNF/proBDNF ratio and FBF (r = 0.64, P < 0.001) and FVR (r = −0.58, P < 0.001) during HG exercise. These results show that peripheral vascular reactivity and serum BDNF responses to exercise training are impaired by the BDNF Val66Met polymorphism and such responsiveness is associated with serum BDNF concentrations in healthy subjects.
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O'Sullivan, E., E. Barrett, S. Grenham, P. Fitzgerald, C. Stanton, R. Ross, E. Quigley, J. Cryan, and T. Dinan. "BDNF expression in the hippocampus of maternally separated rats: does Bifidobacterium breve 6330 alter BDNF levels?" Beneficial Microbes 2, no. 3 (September 1, 2011): 199–207. http://dx.doi.org/10.3920/bm2011.0015.
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Brain-derived neurotrophic factor (BDNF) is of interest because of its putative role in stress and psychiatric disorders. Maternal separation is used as an animal model of early-life stress and of irritable bowel syndrome (IBS). Animals exposed to the paradigm show altered gut function together with heightened levels of arousal and corticosterone. Some probiotic organisms have been shown to be of benefit in IBS and influence the brain-gut axis. Our objective was to investigate the effects of maternal separation on BDNF under basal conditions and in response to the probiotic Bifidobacterium breve 6330. The study implemented the maternal separation model which we have previously described. Polymerase chain reaction and in situ hybridisation were performed to measure the effect of maternal separation on both BDNF total variants and BDNF splice variant (exon) IV in the hippocampus. Maternally separated and non-separated rats were treated with B. breve 6330, to investigate the effect of this probiotic on BDNF total variant and BDNF exon IV expression. Maternal separation increased BDNF total variants (P<0.01), whilst having no effect on BDNF exon IV. B. breve 6330 increased BDNF total variants (P<0.01), and decreased BDNF splice variant IV, in non-separated rats (P<0.01). B. breve 6330 did not alter BDNF levels in the maternally separated rats. Maternal separation caused a marked increase in BDNF in the hippocampus. While B. breve 6330 influenced BDNF in normal animals, it had no significant effect on BDNF in those which were maternally separated. We have demonstrated that an orally administered probiotic can influence hippocampal BDNF.
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Noble, Emily E., Charles J. Billington, Catherine M. Kotz, and ChuanFeng Wang. "The lighter side of BDNF." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 5 (May 2011): R1053—R1069. http://dx.doi.org/10.1152/ajpregu.00776.2010.
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Brain-derived neurotrophic factor (BDNF) mediates energy metabolism and feeding behavior. As a neurotrophin, BDNF promotes neuronal differentiation, survival during early development, adult neurogenesis, and neural plasticity; thus, there is the potential that BDNF could modify circuits important to eating behavior and energy expenditure. The possibility that “faulty” circuits could be remodeled by BDNF is an exciting concept for new therapies for obesity and eating disorders. In the hypothalamus, BDNF and its receptor, tropomyosin-related kinase B (TrkB), are extensively expressed in areas associated with feeding and metabolism. Hypothalamic BDNF and TrkB appear to inhibit food intake and increase energy expenditure, leading to negative energy balance. In the hippocampus, the involvement of BDNF in neural plasticity and neurogenesis is important to learning and memory, but less is known about how BDNF participates in energy homeostasis. We review current research about BDNF in specific brain locations related to energy balance, environmental, and behavioral influences on BDNF expression and the possibility that BDNF may influence energy homeostasis via its role in neurogenesis and neural plasticity.
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Jiang, Yongjun, Ning Wei, Juehua Zhu, Tingting Lu, Zhaoyao Chen, Gelin Xu, and Xinfeng Liu. "Effects of Brain-Derived Neurotrophic Factor on Local Inflammation in Experimental Stroke of Rat." Mediators of Inflammation 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/372423.
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This study was aimed to investigate whether brain-derived neurotrophic factor (BDNF) can modulate local cerebral inflammation in ischemic stroke. Rats were subjected to ischemia by occluding the right middle cerebral artery (MCAO) for 2 hours. Rats were randomized as control, BDNF, and antibody groups. The local inflammation was evaluated on cellular, cytokine, and transcription factor levels with immunofluorescence, enzyme-linked immunosorbent assay, real-time qPCR, and electrophoretic mobility shift assay, respectively. Exogenous BDNF significantly improved motor-sensory, sensorimotor function, and vestibulomotor function, while BDNF did not decrease the infarct volume. Exogenous BDNF increased the number of both activated and phagocytotic microglia in brain. BDNF upregulated interleukin10 and its mRNA expression, while downregulated tumor necrosis factor α and its mRNA expression. BDNF also increased DNA-binding activity of nuclear factor-kappa B. BDNF antibody, which blocked the activity of endogenous BDNF, showed the opposite effect of exogenous BDNF. Our data indicated that BDNF may modulate local inflammation in ischemic brain tissues on the cellular, cytokine, and transcription factor levels.
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Brigadski, Tanja, and Volkmar Leßmann. "The physiology of regulated BDNF release." Cell and Tissue Research 382, no. 1 (September 18, 2020): 15–45. http://dx.doi.org/10.1007/s00441-020-03253-2.
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Abstract The neurotrophic factor BDNF is an important regulator for the development of brain circuits, for synaptic and neuronal network plasticity, as well as for neuroregeneration and neuroprotection. Up- and downregulations of BDNF levels in human blood and tissue are associated with, e.g., neurodegenerative, neurological, or even cardiovascular diseases. The changes in BDNF concentration are caused by altered dynamics in BDNF expression and release. To understand the relevance of major variations of BDNF levels, detailed knowledge regarding physiological and pathophysiological stimuli affecting intra- and extracellular BDNF concentration is important. Most work addressing the molecular and cellular regulation of BDNF expression and release have been performed in neuronal preparations. Therefore, this review will summarize the stimuli inducing release of BDNF, as well as molecular mechanisms regulating the efficacy of BDNF release, with a focus on cells originating from the brain. Further, we will discuss the current knowledge about the distinct stimuli eliciting regulated release of BDNF under physiological conditions.
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Peregud, Danil I., Valeria Yu Baronets, Natalia N. Terebilina, and Natalia V. Gulyaeva. "Role of BDNF in Neuroplasticity Associated with Alcohol Dependence." Biochemistry (Moscow) 88, no. 3 (March 2023): 404–16. http://dx.doi.org/10.1134/s0006297923030094.
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Abstract Chronic alcohol consumption is characterized by disturbances of neuroplasticity. Brain-derived neurotrophic factor (BDNF) is believed to be critically involved in this process. Here we aimed to review actual experimental and clinical data related to BDNF participation in neuroplasticity in the context of alcohol dependence. As has been shown in experiments with rodents, alcohol consumption is accompanied by the brain region-specific changes of BDNF expression and by structural and behavioral impairments. BDNF reverses aberrant neuroplasticity observed during alcohol intoxication. According to the clinical data parameters associated with BDNF demonstrate close correlation with neuroplastic changes accompanying alcohol dependence. In particular, the rs6265 polymorphism within the BDNF gene is associated with macrostructural changes in the brain, while peripheral BDNF concentration may be associated with anxiety, depression, and cognitive impairment. Thus, BDNF is involved in the mechanisms of alcohol-induced changes of neuroplasticity, and polymorphisms within the BDNF gene and peripheral BDNF concentration may serve as biomarkers, diagnostic or prognostic factors in treatment of alcohol abuse.
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Abdollahi, Mona, and Margaret Fahnestock. "Nurr1 Is Not an Essential Regulator of BDNF in Mouse Cortical Neurons." International Journal of Molecular Sciences 23, no. 12 (June 20, 2022): 6853. http://dx.doi.org/10.3390/ijms23126853.
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Nurr1 and brain-derived neurotrophic factor (BDNF) play major roles in cognition. Nurr1 regulates BDNF in midbrain dopaminergic neurons and cerebellar granule cells. Nurr1 and BDNF are also highly expressed in the cerebral cortex, a brain area important in cognition. Due to Nurr1 and BDNF tissue specificity, the regulatory effect of Nurr1 on BDNF in different brain areas cannot be generalized. The relationship between Nurr1 and BDNF in the cortex has not been investigated previously. Therefore, we examined Nurr1-mediated BDNF regulation in cortical neurons in activity-dependent and activity-independent states. Mouse primary cortical neurons were treated with the Nurr1 agonist, amodiaquine (AQ). Membrane depolarization was induced by KCl or veratridine and reversed by nimodipine. AQ and membrane depolarization significantly increased Nurr1 (p < 0.001) and BDNF (pAQ < 0.001, pKCl < 0.01) as assessed by real-time qRT-PCR. However, Nurr1 knockdown did not affect BDNF gene expression in resting or depolarized neurons. Accordingly, the positive correlation between Nurr1 and BDNF expression in AQ and membrane depolarization experiments does not imply co-regulation because Nurr1 knockdown did not affect BDNF gene expression in resting or depolarized cortical neurons. Therefore, in contrast to midbrain dopaminergic neurons and cerebellar granule cells, Nurr1 does not regulate BDNF in cortical neurons.
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Garraway, Sandra M., and J. Russell Huie. "Spinal Plasticity and Behavior: BDNF-Induced Neuromodulation in Uninjured and Injured Spinal Cord." Neural Plasticity 2016 (2016): 1–19. http://dx.doi.org/10.1155/2016/9857201.
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Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family of signaling molecules. Since its discovery over three decades ago, BDNF has been identified as an important regulator of neuronal development, synaptic transmission, and cellular and synaptic plasticity and has been shown to function in the formation and maintenance of certain forms of memory. Neural plasticity that underlies learning and memory in the hippocampus shares distinct characteristics with spinal cord nociceptive plasticity. Research examining the role BDNF plays in spinal nociception and pain overwhelmingly suggests that BDNF promotes pronociceptive effects. BDNF induces synaptic facilitation and engages central sensitization-like mechanisms. Also, peripheral injury-induced neuropathic pain is often accompanied with increased spinal expression of BDNF. Research has extended to examine how spinal cord injury (SCI) influences BDNF plasticity and the effects BDNF has on sensory and motor functions after SCI. Functional recovery and adaptive plasticity after SCI are typically associated with upregulation of BDNF. Although neuropathic pain is a common consequence of SCI, the relation between BDNF and pain after SCI remains elusive. This article reviews recent literature and discusses the diverse actions of BDNF. We also highlight similarities and differences in BDNF-induced nociceptive plasticity in naïve and SCI conditions.
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Fujimura, Hironobu, Ruoyan Chen, Takashi Nakamura, Takeshi Nakahashi, Jun-ichi Kambayashi, Bing Sun, C. Altar, and Narendra Tandon. "Brain-derived Neurotrophic Factor Is Stored in Human Platelets and Released by Agonist Stimulation." Thrombosis and Haemostasis 87, no. 04 (2002): 728–34. http://dx.doi.org/10.1055/s-0037-1613072.
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SummaryBrain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, plays critical roles in the survival, growth, and maintenance of brain and peripheral neurons. We report the presence of BDNF protein in human platelets and its release upon agonist stimulation. The BDNF content of washed platelets varied widely, from 3.5 to 67 ng/ 4 X 108 platelets, averaging 25.2 ± 21.2 ng/4 X 108 platelets (mean ± SD). The BDNF concentration in platelet-poor plasma was low (1.7 ± 1.7 ng/ml, n = 11). Thrombin, collagen, the Ca++ ionophore A23187, and shear stress each induced a rapid release of BDNF from platelets. Up to only half of platelet BDNF was secreted upon agonist stimulation, suggesting that platelets may have a non-releasable pool of BDNF, or that the released BDNF binds to a recognition site on the platelet surface and is internalized, as occurs with serotonin. However, the cognate BDNF receptor, TrkB, was not detected in platelets. Nevertheless, the ability of BDNF to bind washed platelets was shown by FACS analysis confocal microscopy and by the binding and apparent internalization of [125I]-BDNF by platelets. A very high affinity site (Kd = 130 X 10−15 M, ∼80 sites/platelet) and a moderately high affinity site (Kd = 20 nM, ∼3750 sites/platelet) were identified. The BDNF content in two mega-karyocytic cell lines, DAMI and Meg-01, was only 0.1% of the content measured in platelets. No BDNF mRNA was detected by Northern blotting in these cell lines or in platelets. The pituitary gland was also ruled out as a source for platelet BDNF, since the BDNF content of rat platelets did not decrease 2 weeks after hypophysectomy. Thus, platelet BDNF is not acquired from the megakaryocyte or pituitary gland, but is probably acquired from other sources via the blood circulation. Platelets appear to bind, store and release BDNF upon activation at the site of traumatic injury to facilitate the repair of peripheral nerves or other tissues that contain TrkB.
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Zhu, Yanan, Cangang Zhang, Dongyu Zhao, Wenhua Li, Zhe Zhao, Shukun Yao, and Dongyan Zhao. "BDNF Acts as a Prognostic Factor Associated with Tumor-Infiltrating Th2 Cells in Pancreatic Adenocarcinoma." Disease Markers 2021 (November 5, 2021): 1–22. http://dx.doi.org/10.1155/2021/7842035.
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Pancreatic adenocarcinoma (PAAD) is an extremely lethal disease worldwide. Brain-derived neurotrophic factor (BDNF) is a critical member of the neurotrophin polypeptide superfamily that plays an important role in multiple cancers. However, the association among BDNF expression, tumor immunity, and PAAD prognosis remains unclear. BDNF expression and its influence on patient prognosis were explored based on The Cancer Genome Atlas, Cancer Cell Line Encyclopedia, Genotype-Tissue Expression, and Kaplan-Meier plotter. Gene set enrichment analysis was performed to understand the biological roles of BDNF. The role of BDNF in tumor-infiltrating immune cells was determined using the Tumor Immune Estimation Resource database and the single-sample gene set enrichment analysis and xCell algorithm. The correlation among BDNF and chemokines, chemokine receptors, chemotherapeutic efficacy, and immune checkpoints was analyzed based on RStudio. BDNF expression was remarkably higher in PAAD compared to their paired normal tissues, and high BDNF expression was associated with unfavorable prognosis. Enrichment analysis revealed that BDNF was significantly enriched in major oncogenic pathways in PAAD. BDNF expression was positively correlated with immune infiltration, especially Th2 cells. Moreover, BDNF expression was positively correlated with Th2 cell-related chemokine/chemokine receptors, indicating that BDNF might modulate the migration of Th2 cells in PAAD. We also found that BDNF expression was correlated with high chemotherapeutics sensitivity and highly expressed immune checkpoints, making it a valuable biomarker in predicting the therapeutic benefits for chemotherapy and immunotherapy in cancer patients. In summary, BDNF might affect patient prognosis by interacting with tumor-infiltrating Th2 cells, thus serving as a potential prognostic biomarker in PAAD.
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Zheng, Xue, Lu Chen, Tong Chen, Maosheng Cao, Boqi Zhang, Chenfeng Yuan, Zijiao Zhao, Chunjin Li, and Xu Zhou. "The Mechanisms of BDNF Promoting the Proliferation of Porcine Follicular Granulosa Cells: Role of miR-127 and Involvement of the MAPK-ERK1/2 Pathway." Animals 13, no. 6 (March 21, 2023): 1115. http://dx.doi.org/10.3390/ani13061115.
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As a member of the neurotrophic family, brain-derived neurotrophic factor (BDNF) provides a key link in the physiological process of mammalian ovarian follicle development, in addition to its functions in the nervous system. The emphasis of this study lay in the impact of BDNF on the proliferation of porcine follicular granulosa cells (GCs) in vitro. BDNF and tyrosine kinase B (TrkB, receptor of BDNF) were detected in porcine follicular GCs. Additionally, cell viability significantly increased during the culture of porcine GCs with BDNF (100 ng/mL) in vitro. However, BDNF knockdown in GCs decreased cell viability and S-phase cells proportion—and BDNF simultaneously regulated the expression of genes linked with cell proliferation (CCND1, p21 and Bcl2) and apoptosis (Bax). Then, the results of the receptor blocking experiment showed that BDNF promoted GC proliferation via TrkB. The high-throughput sequencing showed that BDNF also regulated the expression profiles of miRNAs in GCs. The differential expression profiles were obtained by miRNA sequencing after BDNF (100 ng/mL) treatment with GCs. The sequencing results showed that, after BDNF treatment, 72 significant differentially-expressed miRNAs were detected—5 of which were related to cell process and proliferation signaling pathways confirmed by RT-PCR. Furthermore, studies showed that BDNF promoted GCs’ proliferation by increasing the expression of CCND1, downregulating miR-127 and activating the ERK1/2 signal pathway. Moreover, BDNF indirectly activated the ERK1/2 signal pathway by downregulating miR-127. In conclusion, BDNF promoted porcine GC proliferation by increasing CCND1 expression, downregulating miR-127 and stimulating the MAPK-ERK1/2 signaling cascade.
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Suriyaprom, Kanjana, Banchamaphon Pheungruang, Somchai Pooudong, Pumpath Putpadungwipon, and Chutima Sirikulchayanonta. "Associations of Plasma BDNF and BDNF Gene Polymorphism with Cardiometabolic Parameters in Thai Children: A Pilot Study." Journal of Nutrition and Metabolism 2023 (March 24, 2023): 1–8. http://dx.doi.org/10.1155/2023/9668626.
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Background. Childhood obesity is an important public health crisis worldwide. The brain-derived neurotrophic factor (BDNF) has been demonstrated to play a role in controlling energy homeostasis and cardiovascular regulation. Objectives. To examine brain-derived neurotrophic factor (BDNF) levels and anthropometric-cardiometabolic and hematological parameters in obese and nonobese children and to determine whether two BDNF gene polymorphisms (G196A and C270T) are linked to BDNF levels, obesity, and anthropometric-cardiometabolic and hematological parameters among Thai children. Methods. This case-control study included an analysis of 469 Thai children: 279 healthy nonobese and 190 obese children. Anthropometric-cardiometabolic and hematological variables and BDNF levels were measured. Genotyping of BDNF G196A and C270T was performed using the polymerase chain reaction-restriction fragment length polymorphism technique. Results. Children in the obese group had significantly higher white blood cell counts and some cardiometabolic parameters. Although the difference in BDNF level between the nonobese and obese groups was not significant, BDNF level was significantly positively correlated with hematological and cardiometabolic parameters, including blood pressure, triglycerides, and triglycerides and the glucose index. The BDNF G196A polymorphism in children was only associated with decreased systolic blood pressure p < 0.05 , while the BDNF C270T polymorphism was found not to be related to BDNF levels, obesity, or other parameters after adjusting for potential covariates. Conclusions. These findings in Thai children suggest that obesity is associated with increased cardiometabolic risk factors, but not with BDNF levels or the two BDNF polymorphisms studied, while the BDNF G196A polymorphism is a beneficial marker for controlling blood pressure among Thai children.
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Kotlega, Dariusz, Agnieszka Zembron-Lacny, Barbara Morawin, Monika Golab-Janowska, Przemyslaw Nowacki, and Malgorzata Szczuko. "Free Fatty Acids and Their Inflammatory Derivatives Affect BDNF in Stroke Patients." Mediators of Inflammation 2020 (December 3, 2020): 1–12. http://dx.doi.org/10.1155/2020/6676247.
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Objective. The neurotrophin brain-derived neurotrophic factor (BDNF) affects poststroke functional outcome, neurogenesis, neuroprotection, and neuroplasticity. Its level is related to the diet and nutritional status, and more specifically, it is free fatty acids (FFAs) and eicosanoids that can have an impact on the BDNF level. The aim of this study was to analyze the potential impact of FFAs and eicosanoids on the BDNF level in stroke patients. Material and Methods. Seventy-three ischemic stroke patients were prospectively enrolled in the study. Laboratory tests were performed in all subjects, including the levels of FFAs, eicosanoids, and BDNF. FFAs and inflammatory metabolites were determined by gas chromatography and liquid chromatography, while BDNF was evaluated by the immune-enzymatic method (ELISA). Results. The plasma level of BDNF negatively correlated with C22:1n9 13 erucic acid, C18:3n3 linolenic acid (ALA), and lipoxin A4 15-epi-LxA4. A direct association was observed in relation to BDNF and C16:1 palmitoleic acid and C20:3n6 eicosatrienoic acid (dihomo-gamma-linolenic acid (DGLA)). Conclusions. Saturated fatty acids and omega-3 and omega-9 erucic acids can affect signaling in the BDNF synthesis resulting in the decrease in BDNF. There is a beneficial effect of DGLA on the BDNF level, while the effect of ALA on BDNF can be inhibitory. Specialized proresolving lipid mediators can play a role in the BDNF metabolism. BDNF can interact with inflammation as the risk factor in the cardiovascular disorders, including stroke.
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Inoue, Yasuhiro, Yoshinaga Okugawa, Susumu Saigusa, Junichiro Hiro, Yuji Toiyama, Koji Tanaka, Yasuhiko Mohri, and Masato Kusunoki. "Effect of brain-derived neurotrophic factor/TrkB axis on cancer progression in colorectal cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e14039-e14039. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14039.
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e14039 Background: Brain-derived neurotrophic factor (BDNF) is one of the member of the neurotropin family known to activate the high affinity tyrosine kinase B (TrkB) receptor together with the pan-neurotropin low-affinity coreceptor p75 (p75NTR). TrkB activation by BDNF has been shown to facilitate the progression of several cancers, however, no reports have shown the clinical and biological effects of BDNF/TrkB axis expression in colorectal cancer(CRC). Methods: A total of 223 consecutive patients undergoing surgery for CRC were enrolled. We analyzed BDNF/TrkB mRNA levels by real-time reverse transcription PCR in CRC tissues, and their relationships with clinicopathological findings including survival were investigated. BDNF and TrkB expression were also evaluated by immunohistochemistry. To investigate the biological role of the BDNF/TrkB axis, recombinant human BDNF and Trk antagonist K252a were used for proliferation, migration, and anoikis assays in CRC cell lines. Results: The mean BDNF level in CRC tissue was 94.3 (0-1326.8). One hundred five of 223 patients (47.1%) showed detectable BDNF levels, whereas the remainder had no detectable. BDNF positive expression was significantly associated with undifferenciated histological type, lymph node metastasis, and hepatic metastasis. In addition, increased BDNF/TrkB axis expression associated with lymph node metastasis, hepatic metastasis, and peritoneal disseamination. Immunohistochemical analysis indicated intense BDNF expression in the cytoplasm of cancer cells, and intense TrkB expression in the nuclei of cancer cells, respectively. In vitro, administration of recombinant human BDNF promoted proliferation, anoikis resistance, and partial migration. These effects were generally inhibited by Trk antagonist K252a. Conclusions: We demonstrated the clinical and biological function of BDNF/TrkB axis in CRC. BDNF/TrkB axis appears to play an important role in cancer progression, and blocking this pathway might be clinically useful in developing therapies for patients with CRC.
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El-Gharbawy, Areeg H., Diane C. Adler-Wailes, Margaret C. Mirch, Kelly R. Theim, Lisa Ranzenhofer, Marian Tanofsky-Kraff, and Jack A. Yanovski. "Serum Brain-Derived Neurotrophic Factor Concentrations in Lean and Overweight Children and Adolescents." Journal of Clinical Endocrinology & Metabolism 91, no. 9 (September 1, 2006): 3548–52. http://dx.doi.org/10.1210/jc.2006-0658.
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Abstract Context: Brain-derived neurotrophic factor (BDNF) and its receptor appear to be important components of the leptin-signaling cascade involved in energy homeostasis, and mice with BDNF or TrkB gene haploinsufficiency have excessive adiposity. Little is known about the relationship between adiposity and BDNF, particularly in children. Objective: The objective of the study was to study the association of serum BDNF with measures of adiposity in children. Design/Setting/Patients: BDNF was determined by a sandwich-type ELISA after an overnight fast in convenience sample of 328 subjects, aged 3–19 yr enriched for extreme obesity. In 43, BDNF was also measured before, and again 1 h after, consuming a high-energy content (787 kcal) milkshake. Main Outcome Measures: Measures included associations between BDNF and measures of adiposity. Results: There were no significant univariate associations between log BDNF and adiposity measured by body mass index (BMI), BMI-Z score, or fat mass. However, in an analysis of covariance accounting for age, sex, race, pubertal status, and platelet count, BDNF was lower in overweight children (mean ± sd, 39.8 ± 24.8 vs. 47.0 ± 25.4 ng/dl, P = 0.03); in multiple regression analyses with log BDNF as the dependent variable, BMI (P = 0.03), BMI-Z (P = 0.01), and body fat (P < 0.02) were all negatively associated with BDNF once age, pubertal status, and platelet count were included in the model. Ingestion of a meal did not significantly alter serum BDNF 1 h later (P = 0.26). Conclusions: Serum BDNF is lower in extremely overweight children and adolescents than those of normal weight. It remains to be determined whether obese individuals with low serum BDNF for age and platelet count have mutations that alter BDNF function.
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Hartmann, David, Jana Drummond, Erik Handberg, Sharday Ewell, and Lucas Pozzo-Miller. "Multiple Approaches to Investigate the Transport and Activity-Dependent Release of BDNF and Their Application in Neurogenetic Disorders." Neural Plasticity 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/203734.
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Studies utilizing genetic and pharmacological manipulations in rodent models and neuronal cultures have revealed myriad roles of brain-derived neurotrophic factor (BDNF). Currently, this knowledge of BDNF function is being translated into improvement strategies for several debilitating neurological disorders in which BDNF abnormalities play a prominent role. Common among the BDNF-related disorders are irregular trafficking and release of mature BDNF (mBDNF) and/or its prodomain predecessor, proBDNF. Thus, investigating the conditions required for proper trafficking and release of BDNF is an essential step toward understanding and potentially improving these neurological disorders. This paper will provide examples of disorders related to BDNF release and serve as a review of the techniques being used to study the trafficking and release of BDNF.
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Pedard, Martin, Céline Brenière, Nicolas Pernet, Catherine Vergely, Yannick Béjot, and Christine Marie. "Brain-derived neurotrophic factor in peripheral blood mononuclear cells and stroke outcome." Experimental Biology and Medicine 243, no. 15-16 (November 2018): 1207–11. http://dx.doi.org/10.1177/1535370218815612.
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Stroke outcome is dependent on brain-derived neurotrophic factor (BDNF)-dependent neuroplasticity. As peripheral blood mononuclear cells (PBMC) contain BDNF, diapedesis of these cells might be followed by BDNF delivery to the ischemic brain. To test this hypothesis, we investigated the association between BDNF levels in PBMC and functional outcome in patients with ischemic stroke. BDNF was measured in PBMC that were isolated from ischemic stroke patients ( n = 40) just before (day 0) and after (days 1 and 3) fibrinolysis. Three months after stroke, patients were stratified using the modified Rankin Scale (mRS) according to the unfavorable (mRS scores 3–6) and favorable (mRS scores 0–2) functional outcome. We used univariate and multivariate logistic regressions to assess the relationship between BDNF levels in PBMC and functional outcome. BDNF levels in PBMC decreased from day 0 to day 3 in patients with unfavorable outcome, while they remained stable in patients with favorable outcome. Patients with favorable outcome exhibited at day 3 higher PBMC-BDNF levels than patients with unfavorable outcome and the levels were associated with good outcome (odd ratio: 12.0; 95% confidence interval, 1.4–106.2, P = 0.023). PBMC-BDNF levels remained a predictor of stroke outcome after adjusting from cardiovascular risk, interval between admission and fibrinolysis, stroke severity from hospital admission to discharge, lymphocytes count, neutrophils/lymphocytes ratio at admission. Favorable functional outcome in ischemic stroke patients that benefited from fibrinolysis was predicted by a high BDNF level in PBMC, suggesting that PBMC might serve as a cellular vector to deliver BDNF to the ischemic brain. Impact statement There are a great number of arguments suggesting that BDNF could be involved in stroke recovery dependent of neuroplasticity. Methods that can enhance BDNF levels in the ischemic brain could therefore have great clinical value. Peripheral blood mononuclear cells (PBMC) that contain BDNF and infiltrate early and sustainably the ischemic brain might be used as a cellular vector to deliver BDNF to the ischemic brain and consequently promote recovery. This work is important in this field to show if this BDNF derived from BDNF could exert a positive action on stroke recovery. Our main results showed that a high BDNF level at day 3 after hospital admission was associated with a 12.4 fold increase in favorable outcome after adjusting for still recognized prognostic markers. The new information in this field is this finding identifies PBMC as an attractive cellular vector to deliver BDNF to the ischemic brain.
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Forsgren, Sture, Ola Grimsholm, Tore Dalén, and Solbritt Rantapää-Dahlqvist. "Measurements in the Blood of BDNF for RA Patients and in Response to Anti-TNF Treatment Help Us to Clarify the Magnitude of Centrally Related Pain and to Explain the Relief of This Pain upon Treatment." International Journal of Inflammation 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/650685.
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Brain-derived neurotrophic factor (BDNF) is a neurotrophin with functions related to neuronal survival/proliferation processes and inflammation. BDNF is also an important central pain mediator. The levels of BDNF have been found to be high for RA patients with severe disease and to become lowered in response to anti-TNF treatment. New information says that the levels of BDNF in the blood parallel the BDNF concentrations in the brain and that BDNF can pass the blood-brain barrier. Furthermore, most of the circulating BDNF is produced in the brain. Habitual and regular exercise, in contrast to temporary exercise, does also lead to a lowering of BDNF blood levels. Both anti-TNF treatment and habitual and regular exercise do have pain-relieving effects. It might be that the pain-relieving effect of anti-TNF treatment is related to an affection of central neuronal regions, hereby influencing BDNF production. Measurements of BDNF in the blood help us to clarify the magnitude of centrally related pain for RA patients and help us to explain the relief of this pain in response to anti-TNF treatment.
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Kumamaru, Emi, Tadahiro Numakawa, Naoki Adachi, Yuki Yagasaki, Aiko Izumi, Madinyet Niyaz, Motoshige Kudo, and Hiroshi Kunugi. "Glucocorticoid Prevents Brain-Derived Neurotrophic Factor-Mediated Maturation of Synaptic Function in Developing Hippocampal Neurons through Reduction in the Activity of Mitogen-Activated Protein Kinase." Molecular Endocrinology 22, no. 3 (March 1, 2008): 546–58. http://dx.doi.org/10.1210/me.2007-0264.
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Abstract An increased level of glucocorticoid may be related to the pathophysiology of depressive disorder. The involvement of brain-derived neurotrophic factor (BDNF) in the antidepressive effect has also been suggested; however, the possible influence of glucocorticoid on the action of BDNF in the developing central nervous system has not been elucidated. In this study, we investigated the effect of glucocorticoid (dexamethasone, DEX) on synaptic maturation and function enhanced by BDNF in early developing hippocampal neurons. In the immature stage, BDNF increased the outgrowth of dendrites and the expression of synaptic proteins including glutamate receptors and presynaptic proteins. Pretreatment with DEX significantly inhibited the BDNF-dependent up-regulation of both dendritic outgrowth and synaptic proteins. In the more mature stage, the BDNF-reinforced postsynaptic Ca2+ influx was decreased by DEX. BDNF-enhanced presynaptic glutamate release was also suppressed. RU486, a glucocorticoid receptor antagonist, canceled the DEX-dependent blocking effect on the action of BDNF. After down-regulation of glucocorticoid receptor by small interfering RNA application, no inhibitory effect of DEX on the BDNF-increased synaptic proteins was observed. Interestingly, the BDNF-activated MAPK/ERK pathway, which is an essential intracellular signaling pathway for the BDNF-increased synaptic proteins, was reduced by DEX. These results suggest that BDNF-mediated synaptic maturation is disturbed after neurons are exposed to high-level glucocorticoid in their development stage.
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Hama, Yuka, Kimiyasu Shiraki, Yoshihiro Yoshida, Atsushi Maruyama, Makoto Yasuda, Masaaki Tsuda, Mariko Honda, et al. "Antibody to Varicella-Zoster Virus Immediate-Early Protein 62 Augments Allodynia in Zoster via Brain-Derived Neurotrophic Factor." Journal of Virology 84, no. 3 (November 18, 2009): 1616–24. http://dx.doi.org/10.1128/jvi.02061-09.
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ABSTRACT Varicella-zoster virus (VZV) expresses immediate-early protein 62 (IE62), and zoster is associated with neuropathic pain. Brain-derived neurotrophic factor (BDNF) is involved in the neuronal mechanism underlying pain hypersensitivity. Zoster is associated with prodrome and the robust production of booster antibody to VZV. We hypothesized that the intrathecal production of antibody to IE62 cross-reacting with BDNF and the nerve injury by skin lesions may augment allodynia in zoster by enhancing BDNF activity. One of three monoclonal antibodies against the 268-556 peptide of IE62 recognized BDNF. Immunological cross-reactivity between IE62 and BDNF and the effects of anti-IE62 monoclonal antibody (anti-IE62 MAb) cross-reactivity with BDNF on BDNF activity in cultured neurons were examined. Anti-IE62 MAb and anti-BDNF MAbs recognized the 414-429 peptide of IE62 and the BDNF dimer. Anti-IE62 MAb significantly augmented BDNF-related transcription in neurons and the morphological development of spinal dorsal horn neurons. Sera from patients recognized IE62 and BDNF and enhanced BDNF activity in neurons. The effect of anti-IE62 antibody on mechanical allodynia was characterized by the threshold of allodynia using von Frey filaments in a spinal nerve injury (SNI) in mice. The administration of anti-IE62 MAb to or immunization with cross-reacting IE62 protein to mice significantly enhanced mechanical allodynia on the side with SNI but not on the uninjured side. Anti-IE62 antibody augmented BDNF activity in neurons and allodynia in mice with SNI. The intrathecal production of anti-IE62 antibody augmenting BDNF activity and peripheral nerve injury by zoster may participate in the pathogenesis of allodynia in zoster.
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Kramer, Bianca M. R., Peter M. J. M. Cruijsen, Debbie T. W. M. Ouwens, Marcel W. Coolen, Gerard J. M. Martens, Eric W. Roubos, and Bruce G. Jenks. "Evidence that Brain-Derived Neurotrophic Factor Acts as an Autocrine Factor on Pituitary Melanotrope Cells of Xenopus laevis." Endocrinology 143, no. 4 (April 1, 2002): 1337–45. http://dx.doi.org/10.1210/endo.143.4.8721.
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Abstract We have investigated the physiological regulation and functional significance of brain-derived neurotrophic factor (BDNF) in the endocrine melanotrope cells of the pituitary pars intermedia of the amphibian Xenopus laevis, which can adapt its skin color to the light intensity of its environment. In black-adapted animals, melanotrope cells produce and release α-melanophore-stimulating hormone (α-MSH). In white-adapted animals, the activity of melanotrope cells is inhibited by neuronal input. Using Western blotting and immunocytochemistry at the light and electron microscopical level, we have detected both the BDNF precursor and the mature BDNF protein in Xenopus melanotrope cells. In situ hybridization and RT-PCR revealed the presence of BDNF mRNA in the pituitary pars intermedia, indicating that BDNF is synthesized in the melanotropes. Real-time quantitative RT-PCR showed that levels of BDNF mRNA in melanotrope cells are about 25 times higher in black- than in white-adapted animals. Although there is no difference in the amount of stored mature BDNF, the amount of BDNF precursor protein is 3.5 times higher in melanotropes of black-adapted animals than in those of white-adapted animals. These data indicate that BDNF mRNA expression and BDNF biosynthesis are up-regulated in active melanotrope cells. Because immunoelectron microscopy showed that BDNF is located in melanotrope secretory granules, BDNF is probably coreleased with α-MSH via the regulated secretory pathway. Superfusion and 3H-amino acid incorporation studies demonstrated that BDNF stimulates the release of α-MSH and the biosynthesis of its precursor protein, POMC. Our results provide evidence that BDNF regulates the activity of Xenopus melanotrope cells in an autocrine fashion.
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McCarthy, Deirdre M., Kaly A. Mueller, Elisa N. Cannon, Megan N. Huizenga, Shayna B. Darnell, Pradeep G. Bhide, and Ghazaleh Sadri-Vakili. "Prenatal Cocaine Exposure Alters BDNF-TrkB Signaling in the Embryonic and Adult Brain." Developmental Neuroscience 38, no. 5 (2016): 365–74. http://dx.doi.org/10.1159/000453609.
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Prenatal cocaine exposure remains a major public health concern because of its adverse effects on cognitive function. Although the molecular mechanisms underlying the cognitive impairment are not fully understood, brain-derived neurotrophic factor (BDNF) signaling via its receptor tyrosine kinase B (TrkB) is emerging as a potential candidate. We used a mouse model to examine the impact of ongoing cocaine exposure on BDNF expression in the dorsal forebrain on embryonic day 15 (E15) as well as the long-term effects of prenatal cocaine exposure on BDNF-TrkB signaling in the frontal cortex in early postnatal (postnatal day 16; P16) and adult (P60) male and female mice. We found that ongoing cocaine exposure decreased BDNF expression in the E15 dorsal forebrain, prenatal cocaine exposure did not alter BDNF or TrkB (total or phosphorylated) expression in the frontal cortex at P16, and that the prenatal cocaine exposure produced significant increases in BDNF, the activated (phosphorylated) form of TrkB, as well as Bdnf mRNA in the frontal cortex at P60. The increase in BDNF protein and mRNA expression at P60 was concurrent with hyperacetylation of histone H3 at the Bdnf promoter in the frontal cortex. The increase in frontal cortical BDNF and activated TrkB at P60 occurred in male but not female mice. Thus, our data demonstrate that ongoing cocaine exposure produces a decrease in BDNF expression in the embryonic brain, and that prenatal cocaine exposure produces a sex-specific increase in frontal cortical BDNF-TrkB signaling at P60 only in male mice. Lastly, hyperacetylation of histone H3 at the Bdnf promoter is one epigenetic mechanism mediating the effects of prenatal cocaine exposure on Bdnf expression at P60 in male mice.
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Lee, S. Y. "The Correlation between Plasma Brain-derived Neurotrophic Factor and Cognitive Function in Bipolar Disorder is Modulated by the BDNF Val66Met Polymorphism." European Psychiatry 41, S1 (April 2017): S76. http://dx.doi.org/10.1016/j.eurpsy.2017.01.243.
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ObjectivesBrain-derived neurotrophic factor (BDNF) may be involved in the pathogenesis of bipolar disorder (BD). The functional BDNF Val66Met polymorphism (rs6265) is associated with secretion of BDNF. The current study aimed to explore the correlation between changes of plasma BDNF and cognitive function after 12 week of treatment, considering the influence of the BDNF val66Met polymorphism. The correlation of changes of plasma BDNF with quality of life (QOL) was explored.MethodsFirst diagnosed patients with BD were recruited. Symptom severity, plasma BDNF levels were examined during weeks 0, 1, 2, 4, 8, and 12. QOL, Wisconsin Card Sorting Test (WCST) and the Conners’ Continuous Performance Test (CPT) were assessed at baseline and endpoint. The genotype of the BDNF Val66Met polymorphism was determined. The change of cognitive function and QOL measures over 12 weeks were reduced by factor analysis. Pearson's correlation was used to investigate the association between change of plasma BDNF levels with cognitive function and QOL.ResultsFive hundred and forty-one BP patients were recruited. Three hundred and fifty-five (65.6%) patients completed the 12-week follow-up. A significant negative correlation was found between changes of plasma BDNF level with factor 1 (WCST) (r = −0.25, P < 0.001). After further stratification according to subtypes of BD and the BDNF genotypes, above significant correlation was found only in those with BP-I and the BDNF Val66Met Val/Met genotype (r = −0.54, P < 0.008).ConclusionWe conclude that changes in plasma BDNF significantly correlated with changes in WCST in patients with BD; such correlation is moderated by the BDNF Val66Met polymorphism and subtype of BD.Disclosure of interestThe author has not supplied his declaration of competing interest.
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Szekeres, Mária, György L. Nádasy, Gábor Turu, Katinka Süpeki, László Szidonya, László Buday, Tracy Chaplin, Adrian J. L. Clark, and László Hunyady. "Angiotensin II-Induced Expression of Brain-Derived Neurotrophic Factor in Human and Rat Adrenocortical Cells." Endocrinology 151, no. 4 (February 24, 2010): 1695–703. http://dx.doi.org/10.1210/en.2009-1060.
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Angiotensin II (Ang II) is a major regulator of steroidogenesis in adrenocortical cells, and is also an effective inducer of cytokine and growth factor synthesis in several cell types. In microarray analysis of H295R human adrenocortical cells, the mRNA of brain-derived neurotrophic factor (BDNF), a neurotrophin widely expressed in the nervous system, was one of the most up-regulated genes by Ang II. The aim of the present study was the analysis of the Ang II-induced BDNF expression and BDNF-induced effects in adrenocortical cells. Real-time PCR studies have shown that BDNF is expressed in H295R and rat adrenal glomerulosa cells. In H295R cells, the kinetics of Ang II-induced BDNF expression was faster than that of aldosterone synthase (CYP11B2). Inhibition of calmodulin kinase by KN93 did not significantly affect the Ang II-induced stimulation of BDNF expression, suggesting that it occurs by a different mechanism from the CYP11B2-response. Ang II also caused candesartan-sensitive, type-1 Ang II receptor-mediated stimulation of BDNF gene expression in primary rat glomerulosa cells. In rat adrenal cortex, BDNF protein was localized to the subcapsular region. Ang II increased BDNF protein levels both in human and rat cells, and BDNF secretion of H295R cells. Ang II also increased type-1 Ang II receptor-mediated BDNF expression in vivo in furosemide-treated rats. In rat glomerulosa cells, BDNF induced tropomyosin-related kinase B receptor-mediated stimulation of EGR1 and TrkB expression. These data demonstrate that Ang II stimulates BDNF expression in human and rat adrenocortical cells, and BDNF may have a local regulatory function in adrenal glomerulosa cells.
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Matsumoto, Tomoya, Stefanie Rauskolb, Martin Polack, Johannes Klose, Roland Kolbeck, Martin Korte, and Yves-Alain Barde. "Biosynthesis and processing of endogenous BDNF: CNS neurons store and secrete BDNF, not pro-BDNF." Nature Neuroscience 11, no. 2 (January 20, 2008): 131–33. http://dx.doi.org/10.1038/nn2038.
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Gustafsson, David, Andrea Klang, Sebastian Thams, and Elham Rostami. "The Role of BDNF in Experimental and Clinical Traumatic Brain Injury." International Journal of Molecular Sciences 22, no. 7 (March 30, 2021): 3582. http://dx.doi.org/10.3390/ijms22073582.
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Traumatic brain injury is one of the leading causes of mortality and morbidity in the world with no current pharmacological treatment. The role of BDNF in neural repair and regeneration is well established and has also been the focus of TBI research. Here, we review experimental animal models assessing BDNF expression following injury as well as clinical studies in humans including the role of BDNF polymorphism in TBI. There is a large heterogeneity in experimental setups and hence the results with different regional and temporal changes in BDNF expression. Several studies have also assessed different interventions to affect the BDNF expression following injury. Clinical studies highlight the importance of BDNF polymorphism in the outcome and indicate a protective role of BDNF polymorphism following injury. Considering the possibility of affecting the BDNF pathway with available substances, we discuss future studies using transgenic mice as well as iPSC in order to understand the underlying mechanism of BDNF polymorphism in TBI and develop a possible pharmacological treatment.
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Lai, Ning-Sheng, Hui-Chun Yu, Hsien-Yu Huang Tseng, Chia-Wen Hsu, Hsien-Bin Huang, and Ming-Chi Lu. "Increased Serum Levels of Brain-Derived Neurotrophic Factor Contribute to Inflammatory Responses in Patients with Rheumatoid Arthritis." International Journal of Molecular Sciences 22, no. 4 (February 12, 2021): 1841. http://dx.doi.org/10.3390/ijms22041841.
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The aim of this study is to investigate the role of brain-derived neurotrophic factor (BDNF) in the inflammatory responses in patients with rheumatoid arthritis (RA). Serum levels of BDNF and the precursor form of BDNF (proBDNF) from 625 RA patients and 40 controls were analyzed using enzyme-linked immunosorbent assay. Effects of BDNF on the mitogen-activated protein kinase pathway were analyzed by Western blotting. Microarray analysis was conducted to search BDNF regulated gene expression in Jurkat cells, and the differentially expressed genes were validated using T cells from patients with RA and controls. Serum BDNF levels were significantly elevated in patients with RA compared with the controls. Low serum BDNF levels were found in RA patients with anxiety or receiving biologics treatment. BDNF (20 ng/mL) enhanced the phosphorylation of ERK, JNK, and c-Jun, but suppressed the phosphorylation of p38, whereas BDNF (200 ng/mL) enhanced the phosphorylation of ERK and p38. After validation, the expression of CAMK2A, MASP2, GNG13, and MUC5AC, regulated by BDNF and one of its receptors, NGFR, was increased in RA T cells. BDNF increased the IL-2, IL-17, and IFN-γ expression in Jurkat cells and IL-2 and IFN-γ secretion in activated peripheral blood mononuclear cells.
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Loy, Thomas Leonhard, David Vehlow, Vivien Kauschke, Martin Müller, Christian Heiss, and Katrin Susanne Lips. "Effects of BDNF and PEC Nanoparticles on Osteocytes." Molecules 25, no. 18 (September 10, 2020): 4151. http://dx.doi.org/10.3390/molecules25184151.
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Bone substitute materials loaded with mediators that stimulate fracture healing are demanded in the clinical treatment in trauma surgery and orthopedics. Brain-derived neurotrophic factor (BDNF) enhances the proliferation and differentiation of mesenchymal stem cells into osteoblast. To load the implants with BDNF, a drug delivery system that allows the release of BDNF under spatiotemporal control would improve functionality. Polyelectrolyte complex nanoparticles (PECNP) have been reported as a suitable drug delivery system. The suitability of PECNP in contact with osteocytes as the main cell type of bone is not known so far. Thus, we aimed to verify that BDNF and PECNP loaded with BDNF (PECNP+BDNF) as well as pure PECNP have no negative effects on osteocytes in vitro. Therefore, the murine osteocyte cell line MLO-Y4 was treated with BDNF and PECNP+BDNF. The effects on proliferation were analyzed by the BrdU test (n = 5). The results demonstrated a significant increase in proliferation 24 h after BDNF application, whereas PECNP+BDNF did not lead to significant changes. Thus, we conclude that BDNF is an appropriate mediator to stimulate osteocytes. Since the addition of PECNP did not affect the viability of osteocytes, we conclude that PECNP are a suitable drug delivery system for bone implants.
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Latomme, Julie, Patrick Calders, Hilde Van Waelvelde, Tineke Mariën, and Marieke De Craemer. "The Role of Brain-Derived Neurotrophic Factor (BDNF) in the Relation between Physical Activity and Executive Functioning in Children." Children 9, no. 5 (April 22, 2022): 596. http://dx.doi.org/10.3390/children9050596.
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Physical activity (PA) can improve children’s executive functioning (EF), which might be caused by increased levels of brain-derived neurotrophic factor (BDNF). This study investigated whether acute and/or chronic PA leads to increased BDNF levels and enhanced EF in children. Methods: In total, 47 children (mean age 9.69 ± 0.60; 46.8% boys) participated. Children performed a maximal exercise test to measure acute PA. Before and after, BDNF was collected and EF was measured. Chronic PA was proxy-reported. Repeated Measures ANOVAs were performed to study the effect of acute PA on BDNF and EF. Mediation analyses were performed to investigate the mediation effect of BDNF on the association between chronic PA and BDNF. Results: A borderline significant effect of acute PA on BDNF was found (F = 3.32, p = 0.075) with an increase in BDNF (+29.58 pg/mL) after acute PA. A significant effect was found for performance on inhibition tasks (Flanker (accuracy +5.67%, p = 0.034) and Go/No-Go (+0.15%, p = 0.022)). No effect of acute PA was found on the EF outcomes. No significant correlation between chronic PA and EFs nor BDNF was found. Conclusions: Acute PA might increase BDNF and improve some EFs (i.e., inhibition) in children. Chronic PA was not associated with EF nor BDNF. Trial Registration Number: NCT02503579.