Relevant bibliographies by topics / Stem cells, VEGF signaling, Neuropathic pain

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Academic literature on the topic 'Stem cells, VEGF signaling, Neuropathic pain'

Author: Grafiati
Published: 10 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "Stem cells, VEGF signaling, Neuropathic pain"

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Osthues, Tabea, Béla Zimmer, Vittoria Rimola, Kevin Klann, Karin Schilling, Praveen Mathoor, Carlo Angioni, et al. "The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain." Cells 9, no. 7 (July 21, 2020): 1740. http://dx.doi.org/10.3390/cells9071740.

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Nerve injury-induced neuropathic pain is difficult to treat and mechanistically characterized by strong neuroimmune interactions, involving signaling lipids that act via specific G-protein coupled receptors. Here, we investigated the role of the signaling lipid receptor G2A (GPR132) in nerve injury-induced neuropathic pain using the robust spared nerve injury (SNI) mouse model. We found that the concentrations of the G2A agonist 9-HODE (9-Hydroxyoctadecadienoic acid) are strongly increased at the site of nerve injury during neuropathic pain. Moreover, G2A-deficient mice show a strong reduction of mechanical hypersensitivity after nerve injury. This phenotype is accompanied by a massive reduction of invading macrophages and neutrophils in G2A-deficient mice and a strongly reduced release of the proalgesic mediators TNFα, IL-6 and VEGF at the site of injury. Using a global proteome analysis to identify the underlying signaling pathways, we found that G2A activation in macrophages initiates MyD88-PI3K-AKT signaling and transient MMP9 release to trigger cytoskeleton remodeling and migration. We conclude that G2A-deficiency reduces inflammatory responses by decreasing the number of immune cells and the release of proinflammatory cytokines and growth factors at the site of nerve injury. Inhibiting the G2A receptor after nerve injury may reduce immune cell-mediated peripheral sensitization and may thus ameliorate neuropathic pain.
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Bandovkina, Valeria A., Elena M. Frantsiyants, Ludmila Ya Rozenko, Viktoria V. Pozdnyakova, Natalia D. Cheryarina, Yuriy V. Przhedetskiy, Olga V. Khokhlova, Viktoria Yu Przhedetskaya, Natalia A. Zakharova, and Oleg I. Kit. "Chronic neurogenic pain activates growth factors in the blood of patients with cutaneous melanoma." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e22082-e22082. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e22082.

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e22082 Background: Clusters of tumor cells in blood vessels secrete VEGF family factors necessary for the formation of premetastatic niches. TGF-β activates the epidermal-mesenchymal transition (EMT). The purpose of the study was to analyze levels of angiogenesis and EMT factors in the blood of patients with cutaneous melanoma (M) and chronic neurogenic pain (CNP). Methods: Blood levels of VEGF-A, VEGF-C, VEGFR-1, VEGFR-3, TGF-β1 and TGF-βR2 were measured by ELISA in patients with Т3-4NxM0 melanoma: 21 women with CNP (pelvic pain - 7, osteochondrosis – 14), mean age 67.2±2.7 years; 17 men with CNP (osteochondrosis), mean age 65.6±3.1 years. The control group included patients with melanoma similar in age, gender and disease stages without CNP. Results: VEGF-A in women and men with M+CNP was higher than in controls by 2.7 and 24.9 times respectively; VEGFR-1 was decreased in women by 1.8 times and increased in men by 1.8 times. VEGF-С was unchanged in women and 1.5 times higher in men, and VEGFR-3 was increased by 2.2 times in women and unchanged in men. TGF-β1 was elevated in women and men with M+CNP by 1.4 and 1.8 times, compared to controls, TGF-βR2 – by 1.9 and 2 times respectively. Conclusions: In the blood of women with M+CNP, CNP activates the blood vascular endothelial growth factor VEGF-A and the factor of epidermal-mesenchymal transition TGF-β, while in the blood of men with M+CNP it activates the blood vascular endothelial growth factor VEGF-A, the lymphatic vascular endothelial growth factor VEGF-C and the factor of epidermal-mesenchymal transition TGF-β. VEGF mediates vascular permeability and is associated with the mobilization of endothelial progenitor cells from the bone marrow into premetastatic niches. Activation of TGF-β signaling promotes the induction of the epidermal-mesenchymal transition and supports the properties of cancer stem cells.
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Xie, Junran, Jinxuan Ren, Na Liu, Chengwei Wu, Dongju Xiao, Huanyu Luo, and Jingxian Du. "Pretreatment with AM1241 Enhances the Analgesic Effect of Intrathecally Administrated Mesenchymal Stem Cells." Stem Cells International 2019 (September 10, 2019): 1–17. http://dx.doi.org/10.1155/2019/7025473.

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Mesenchymal stem cells have cannabinoid (CB) receptors type 1 and type 2 and can alleviate a variety of neuropathic pains, including chronic constriction injury (CCI). A selective CB2 receptor agonist is AM1241. In the present study, it was found that mice with CCI displayed a longer duration of mechanical and thermal analgesia when intrathecally (i.t.) injected with AM1241-treated mesenchymal stem cells, compared to those injected with untreated mesenchymal stem cells or AM1241 alone. Moreover, CCI-induced upregulation of the phosphorylated extracellular signal-regulated kinase (ERK) 1/2 (p-ERK1/2) was inhibited following i.t. injection of AM1241-treated mesenchymal stem cells and this inhibition was noticeably higher compared to injection with untreated mesenchymal stem cells. The expression of transforming growth factor-β1 (TGF-β1) was also analyzed in the dorsal root ganglion (DRGs) and spinal cord of CCI mice. In untreated CCI mice, expression of TGF-β1 was increased, whereas pretreatment with AM1241-treated mesenchymal stem cells regulated the expression of TGF-β1 on 10 days and 19 days after surgery. In addition, i.t. injection of exogenous TGF-β1 slightly alleviated neuropathic pain whilst neutralization of TGF-β1 potently blocked the effect of AM1241-treated mesenchymal stem cells on thermal hyperalgesia and mechanical allodynia of CCI mice. In an in vitro experiment, AM1241 could enhance the release of TGF-β1 in the supernatant of BMSCs after lipopolysaccharide (LPS) simulation. Taken together, the findings of the current study show that i.t. administration of AM1241-treated mesenchymal stem cells has a positive effect on analgesia and that TGF-β1 and p-ERK1/2 may be the molecular signaling pathway involved in this process.
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Negri, Lucia, and Napoleone Ferrara. "The Prokineticins: Neuromodulators and Mediators of Inflammation and Myeloid Cell-Dependent Angiogenesis." Physiological Reviews 98, no. 2 (April 1, 2018): 1055–82. http://dx.doi.org/10.1152/physrev.00012.2017.

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The mammalian prokineticins family comprises two conserved proteins, EG-VEGF/PROK1 and Bv8/PROK2, and their two highly related G protein-coupled receptors, PKR1 and PKR2. This signaling system has been linked to several important biological functions, including gastrointestinal tract motility, regulation of circadian rhythms, neurogenesis, angiogenesis and cancer progression, hematopoiesis, and nociception. Mutations in PKR2 or Bv8/PROK2 have been associated with Kallmann syndrome, a developmental disorder characterized by defective olfactory bulb neurogenesis, impaired development of gonadotropin-releasing hormone neurons, and infertility. Also, Bv8/PROK2 is strongly upregulated in neutrophils and other inflammatory cells in response to granulocyte-colony stimulating factor or other myeloid growth factors and functions as a pronociceptive mediator in inflamed tissues as well as a regulator of myeloid cell-dependent tumor angiogenesis. Bv8/PROK2 has been also implicated in neuropathic pain. Anti-Bv8/PROK2 antibodies or small molecule PKR inhibitors ameliorate pain arising from tissue injury and inhibit angiogenesis and inflammation associated with tumors or some autoimmune disorders.
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Yamamizu, Kohei, Sadayoshi Furuta, Shiori Katayama, Michiko Narita, Naoko Kuzumaki, Satoshi Imai, Hiroshi Nagase, Tsutomu Suzuki, Minoru Narita, and Jun K. Yamashita. "The κ opioid system regulates endothelial cell differentiation and pathfinding in vascular development." Blood 118, no. 3 (July 21, 2011): 775–85. http://dx.doi.org/10.1182/blood-2010-09-306001.

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Abstract The opioid system (opioid peptides and receptors) regulates a variety of neurophysiologic functions, including pain control. Here we show novel roles of the κ opioid system in vascular development. Previously, we revealed that cAMP/protein kinase A (PKA) signaling enhanced differentiation of vascular progenitors expressing VEGF receptor-2 (fetal liver kinase 1; Flk1) into endothelial cells (ECs) through dual up-regulation of Flk1 and Neuropilin1 (NRP1), which form a selective and sensitive VEGF164 receptor. Kappa opioid receptor (KOR), an inhibitory G protein–coupled receptor, was highly expressed in embryonic stem cell–derived Flk1+ vascular progenitors. The addition of KOR agonists to Flk1+ vascular progenitors inhibited EC differentiation and 3-dimensional vascular formation. Activation of KOR decreased expression of Flk1 and NRP1 in vascular progenitors. The inhibitory effects of KOR were reversed by 8-bromoadenosine-3′,5′-cAMP or a PKA agonist, N6-benzoyl-cAMP, indicating that KOR inhibits cAMP/PKA signaling. Furthermore, KOR-null or dynorphin (an endogenous KOR agonist)–null mice showed a significant increase in overall vascular formation and ectopic vascular invasion into somites at embryonic day −10.5. ECs in these null mice showed significant increase in Flk1 and NRP1, along with reciprocal decrease in plexinD1, which regulates vascular pathfinding. The opioid system is, thus, a new regulator of vascular development that simultaneously modifies 2 distinct vascular properties, EC differentiation and vascular pathfinding.
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Berenson, James R., Thomas Ervin, Ralph V. Boccia, Olcay Batuman, Regina Swift, Christina DiLauro Abaya, Andrew P. Mazar, Gilad S. Gordon, Steven D. Reich, and Jennifer A. Callahan. "Results from the Phase I Portion of a Phase I/II Study of ATN-224 and Bortezomib for Patients with Multiple Myeloma Relapsed from or Refractory to Bortezomib." Blood 112, no. 11 (November 16, 2008): 5185. http://dx.doi.org/10.1182/blood.v112.11.5185.5185.

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Abstract ATN-224 (bis-choline tetrathiomolybdate) is an orally-available small molecule that is currently being studied in several phase II oncology clinical trials. ATN-224 inhibits copper-zinc superoxide dismutase (Cu/Zn-SOD; SOD1) in endothelial and tumor cells. SOD1 is an enzyme that mediates signaling by a number of mitogens including VEGF, FGF-2, EGF, IGF-1 and PDGF. The inhibition of SOD1 by ATN-224 leads to the inhibition of proliferation in endothelial cells and the induction of apoptosis in tumor cells. In a preclinical mouse model using multiple myeloma (MM) cells obtained from a patient that was refractory to bortezomib, the combination of ATN-224 and bortezomib was more effective than either agent alone and led to tumor regression. Based on this data, a phase I/II clinical study evaluating the combination of ATN-224 and bortezomib for MM patients that had previously failed bortezomib was initiated. The phase I portion of this study evaluated the safety of several doses of both ATN-224 and bortezomib and established a recommended dose and schedule of this combination for the phase II portion of the study. The phase I study has completed enrollment and results are presented here. Patients with recurrent or refractory MM that had previously failed bortezomib and currently showing evidence of disease progression were enrolled. Patients had adequate ECOG performance status (PS 0–2) and hematologic and organ function. Patients were monitored for safety and preliminary evidence of efficacy. Blood samples were collected at specific intervals for pharmacokinetic and pharmacodynamic analyses. Twenty-one patients (62% male), aged 46–80 (mean 66) with PS 0–1 were enrolled into 6 cohorts. Dose Limiting Toxicity (DLT) was defined as grade 3 or 4 neutropenia with neutropenic fever, grade 4 neutropenia, grade 3 or 4 thrombocytopenia, grade 2 peripheral neuropathy with pain, grade 3 or 4 neuropathic pain and/or peripheral sensory neuropathy, grade 4 anemia or a fall in hemoglobin by >3 g/dL when day 1 hemoglobin is ≥11 g/dL or >2 g/dL when day 1 hemoglobin is <11 g/dL over a 28-day interval, or any grade 3 or 4 non-hematologic treatment-related toxicity (excluding alopecia) that cannot be reduced to grade 2 or less with symptomatic therapy within 7 days. In the initial 3 cohorts of the trial (n=10), ATN-224 was administered at doses of either 240, 180, or 210 mg daily in combination with bortezomib at a dose of 0.7 mg/m2/dose on days 1, 4, 8 and 11 of a 21 day cycle. Several DLTs [hemoglobin decreased >2g/dL from baseline (n=3) and grade 3 fatigue (n=1)] were observed within the first three cohorts. After review of this data, it was determined that the more appropriate dosing schedule included a 7 day drug holiday. In cohorts 4 through 6 (n=11), ATN-224 was administered at doses of either 180 or 210 mg daily for 21 days in combination with bortezomib at a dose of either 1.0 or 1.3 mg/m2/dose on days 8,11, 15 and 18 of a 28 day cycle. One DLT (grade 4 thrombocytopenia) was observed and occurred in the 180 mg ATN-224 plus 1.3mg/m2/dose bortezomib cohort. By incrementally increasing each dose of ATN-224 and bortezomib individually and modifying the treatment schedule, treatment-related toxicities have been minimized while maximizing the treatment doses. One patient experienced a complete response that was durable for over 10 months. The other 20 patients experienced disease progression within 90 days. A daily dose of 210 mg of ATN-224 for 21 days and a dose of bortezomib at 1.0 mg/m2 on days 8, 11, 15, and 18 of a 28 day cycle was well tolerated and recommended for the phase II portion of this trial, which is now enrolling patients. The phase I portion of the study demonstrates that the combination of ATN-224 and bortezomib can be safely administered and may be an effective treatment for MM patients that are relapsed from or refractory to bortezomib.
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Gowran, A., T. Kulikova, FC Lewis, G. Foldes, L. Fuentes, LE Viiri, V. Spinelli, et al. "Poster session 3Cell growth, differentiation and stem cells - Heart511The role of the endocannabinoid system in modelling muscular dystrophy cardiac disease with induced pluripotent stem cells.512An emerging role of T lymphocytes in cardiac regenerative processes in heart failure due to dilated cardiomyopathy513Canonical wnt signaling reverses the ‘aged/senescent’ human endogenous cardiac stem cell phenotype514Hippo signalling modulates survival of human induced pluripotent stem cell-derived cardiomyocytes515Biocompatibility of mesenchymal stem cells with a spider silk matrix and its potential use as scaffold for cardiac tissue regeneration516A snapshot of genome-wide transcription in human induced pluripotent stem cell-derived hepatocyte-like cells (iPSC-HLCs)517Can NOS/sGC/cGK1 pathway trigger the differentiation and maturation of mouse embryonic stem cells (ESCs)?518Introduction of external Ik1 to human-induced pluripotent stem cell-derived cardiomyocytes via Ik1-expressing HEK293519Cell therapy of the heart studied using adult myocardial slices in vitro520Enhancement of the paracrine potential of human adipose derived stem cells when cultured as spheroid bodies521Mechanosensitivity of cardiomyocyte progenitor cells: the strain response in 2D and 3D environments522The effect of the vascular-like network on the maturation of the human induced pluripotent stem cell derived cardiomyocytes.Transcriptional control and RNA species - Heart525Gene expression regulation in heart failure: from pathobiology to bioinformatics526Human transcriptome in idiopathic dilated cardiomyopathy - a novel high throughput screening527A high-throghput approach unveils putative miRNA-mediated mitochondria-targeted cardioprotective circuits activated by T3 in the post ischemia reperfusion setting528The effect of uraemia on the expression of miR-212/132 and the calcineurin pathway in the rat heartCytokines and cellular inflammation - Heart531Lack of growth differentiation factor 15 aggravates adverse cardiac remodeling upon pressure-overload in mice532Blocking heteromerization of platelet chemokines ccl5 and cxcl4 reduces inflammation and preserves heart function after myocardial infarction533Is there an association between low-dose aspirin use and clinical outcome in HFPEF? Implications of modulating monocyte function and inflammatory mediator release534N-terminal truncated intracellular matrix metalloproteinase-2 expression in diabetic heart.535Expression of CD39 and CD73 on peripheral T-cell subsets in calcific aortic stenosis536Mast cells in the atrial myocardium of patients with atrial fibrillation: a comparison with patients in sinus rhythm539Characteristics of the inflammatory response in patients with coronary artery disease and arterial hypertension540Pro-inflammatory cytokines as cardiovascular events predictors in rheumatoid arthritis and asymptomatic atherosclerosis541Characterization of FVB/N murinic bone marrow-derived macrophage polarization into M1 and M2 phenotypes542The biological expression and thoracic anterior pain syndromeSignal transduction - Heart545The association of heat shock protein 90 and TGFbeta receptor I is involved in collagen production during cardiac remodelling in aortic-banded mice546Loss of the inhibitory GalphaO protein in the rostral ventrolateral medulla of the brainstem leads to abnormalities in cardiovascular reflexes and altered ventricular excitablitiy547Selenoprotein P regulates pressure overload-induced cardiac remodeling548Study of adenylyl cyclase activity in erythrocyte membranes in patients with chronic heart failure549Direct thrombin inhibitors inhibit atrial myocardium hypertrophy in a rat model of heart failure and atrial remodeling550Tissue factor / FVIIa transactivates the IGF-1R by a Src-dependent phosphorylation of caveolin-1551Notch signaling is differently altered in endothelial and smooth muscle cells of ascending aortic aneurysm patients552Frizzled 5 expression is essential for endothelial proliferation and migration553Modulation of vascular function and ROS production by novel synthetic benzopyran analogues in diabetes mellitusExtracellular matrix and fibrosis - Heart556Cardiac fibroblasts as inflammatory supporter cells trigger cardiac inflammation in heart failure557A role for galectin-3 in calcific aortic valve stenosis558Omega-3 polyunsaturated fatty acids- can they decrease risk for ventricular fibrillation?559Serum levels of elastin derived peptides and circulating elastin-antielastin immune complexes in sera of patients with coronary artery disease560Endocardial fibroelastosis is secondary to hemodynamic alterations in the chick model of hypoplastic left heart syndrome561Dynamics of serum levels of matrix metalloproteinases in primary anterior STEMI patients564Deletion of the alpha-7 nicotinic acetylcholine receptor changes the vascular remodeling induced by transverse aortic constriction in mice.565Extracellular matrix remodelling in response to venous hypertension: proteomics of human varicose veinsIon channels, ion exchangers and cellular electrophysiology - Heart568Microtubule-associated protein RP/EB family member 1 modulates sodium channel trafficking and cardiac conduction569Investigation of electrophysiological abnormalities in a rabbit athlete's heart model570Upregulation of expression of multiple genes in the atrioventricular node of streptozotocin-induced diabetic rat571miR-1 as a regulator of sinoatrial rhythm in endurance training adaptation572Selective sodium-calcium exchanger inhibition reduces myocardial dysfunction associated with hypokalaemia and ventricular fibrillation573Effect of racemic and levo-methadone on action potential of human ventricular cardiomyocytes574Acute temperature effects on the chick embryonic heart functionVasculogenesis, angiogenesis and arteriogenesis577Clinical improvement and enhanced collateral vessel growth after monocyte transplantation in mice578The role of HIF-1 alpha, VEGF and obstructive sleep apnoea in the development of coronary collateral circulation579Initiating cardiac repair with a trans-coronary sinus catheter intervention in an ischemia/reperfusion porcine animal model580Early adaptation of pre-existing collaterals after acute arteriolar and venular microocclusion: an in vivo study in chick chorioallantoic membraneEndothelium583EDH-type responses to the activator of potassium KCa2.3 and KCa3.1 channels SKA-31 in the small mesenteric artery from spontaneously hypertensive rats584The peculiarities of endothelial dysfunction in patients with chronic renocardial syndrome585Endothelial dysfunction, atherosclerosis of the carotid arteries and level of leptin in patient with coronary heart disease in combination with hepatic steatosis depend from body mass index.586Role of non-coding RNAs in thoracic aortic aneurysm associated with bicuspid aortic valve587Cigarette smoke extract abrogates atheroprotective effects of high laminar flow on endothelial function588The prognostic value of anti-connective tissue antibodies in coronary heart disease and asymptomatic atherosclerosis589Novel potential properties of bioactive peptides from spanish dry-cured ham on the endothelium.Lipids592Intermediate density lipoprotein is associated with monocyte subset distribution in patients with stable atherosclerosis593The characteristics of dyslipidemia in rheumatoid arthritisAtherosclerosis596Macrophages differentiated in vitro are heterogeneous: morphological and functional profile in patients with coronary artery disease597Palmitoylethanolamide promotes anti-inflammatory phenotype of macrophages and attenuates plaque formation in ApoE-/- mice598Amiodarone versus esmolol in the perioperative period: an in vitro study of coronary artery bypass grafts599BMPRII signaling of fibrocytes, a mesenchymal progenitor cell population, is increased in STEMI and dyslipidemia600The characteristics of atherogenesis and systemic inflammation in rheumatoid arthritis601Role of adenosine-to-inosine RNA editing in human atherosclerosis602Presence of bacterial DNA in thrombus aspirates of patients with myocardial infarction603Novel E-selectin binding polymers reduce atherosclerotic lesions in ApoE(-/-) mice604Differential expression of the plasminogen receptor Plg-RKT in monocyte and macrophage subsets - possible functional consequences in atherogenesis605Apelin-13 treatment enhances the stability of atherosclerotic plaques606Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and favor atherosclerotic plaque instability607Association of neutrophil to lymphocyte ratio with presence of isolated coronary artery ectasiaCalcium fluxes and excitation-contraction coupling610The coxsackie- and adenovirus receptor (CAR) regulates calcium homeostasis in the developing heart611HMW-AGEs application acutely reduces ICaL in adult cardiomyocytes612Measuring electrical conductibility of cardiac T-tubular systems613Postnatal development of cardiac excitation-contraction coupling in rats614Role of altered Ca2+ homeostasis during adverse cardiac remodeling after ischemia/reperfusion615Experimental study of sarcoplasmic reticulum dysfunction and energetic metabolism in failing myocardium associated with diabetes mellitusHibernation, stunning and preconditioning618Volatile anesthetic preconditioning attenuates ischemic-reperfusion injury in type II diabetic patients undergoing on-pump heart surgery619The effect of early and delayed phase of remote ischemic preconditioning on ischemia-reperfusion injury in the isolated hearts of healthy and diabetic rats620Post-conditioning with 1668-thioate leads to attenuation of the inflammatory response and remodeling with less fibrosis and better left ventricular function in a murine model of myocardial infarction621Maturation-related changes in response to ischemia-reperfusion injury and in effects of classical ischemic preconditioning and remote preconditioningMitochondria and energetics624Phase changes in myocardial mitochondrial respiration caused by hypoxic preconditioning or periodic hypoxic training625Desmin mutations depress mitochondrial metabolism626Methylene blue modulates mitochondrial function and monoamine oxidases-related ROS production in diabetic rat hearts627Doxorubicin modulates the real-time oxygen consumption rate of freshly isolated adult rat and human ventricular cardiomyocytesCardiomyopathies and fibrosis630Effects of genetic or pharmacologic inhibition of the ubiquitin/proteasome system on myocardial proteostasis and cardiac function631Suppression of Wnt signalling in a desmoglein-2 transgenic mouse model for arrhythmogenic cardiomyopathy632Cold-induced cardiac hypertrophy is reversed after thermo-neutral deacclimatization633CD45 is a sensitive marker to diagnose lymphocytic myocarditis in endomyocardial biopsies of living patients and in autopsies634Atrial epicardial adipose tissue derives from epicardial progenitors635Caloric restriction ameliorates cardiac function, sympathetic cardiac innervation and beta-adrenergic receptor signaling in an experimental model of post-ischemic heart failure636High fat diet improves cardiac remodelling and function after extensive myocardial infarction in mice637Epigenetic therapy reduces cardiac hypertrophy in murine models of heart failure638Imbalance of the VHL/HIF signaling in WT1+ Epicardial Progenitors results in coronary vascular defects, fibrosis and cardiac hypertrophy639Diastolic dysfunction is the first stage of the developing heart failure640Colchicine aggravates coxsackievirus B3 infection in miceArterial and pulmonary hypertension642Osteopontin as a marker of pulmonary hypertension in patients with coronary heart disease combined with chronic obstructive pulmonary disease643Myocardial dynamic stiffness is increased in experimental pulmonary hypertension partly due to incomplete relaxation644Hypotensive effect of quercetin is possibly mediated by down-regulation of immunotroteasome subunits in aorta of spontaneously hypertensive rats645Urocortin-2 improves right ventricular function and attenuates experimental pulmonary arterial hypertension646A preclinical evaluation of the anti-hypertensive properties of an aqueous extract of Agathosma (Buchu)Biomarkers648The adiponectin level in hypertensive females with rheumatoid arthritis and its relationship with subclinical atherosclerosis649Markers for identification of renal dysfunction in the patients with chronic heart failure650cardio-hepatic syndromes in chronic heart failure: North Africa profile651To study other biomarkers that assess during myocardial infarction652Interconnections of apelin levels with parameters of lipid metabolism in hypertension patients653Plasma proteomics in hypertension: prediction and follow-up of albuminuria during chronic renin-angiotensin system suppression654Soluble RAGE levels in plasma of patients with cerebrovascular events." Cardiovascular Research 111, suppl 1 (July 1, 2016): S92—S116. http://dx.doi.org/10.1093/cvr/cvw150.

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Liu, Yujie, Lu Feng, Shichao Ren, Yingxiu Zhang, and Jing Xue. "Inhibition of lncRNA DILC attenuates neuropathic pain via the SOCS3/JAK2/STAT3 pathway." Bioscience Reports 40, no. 6 (June 2020). http://dx.doi.org/10.1042/bsr20194486.

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Abstract Long noncoding RNAs (lncRNAs) have been involved in the development of multiple pathological processes including neuropathic pain. The aim of the present study is to investigate the role of lncRNA down-regulated in liver cancer stem cells (DILC) in the progression of neuropathic pain and its underlying mechanism. Neuropathic pain rat model was established with the bilateral chronic constriction injury (bCCI) method. The results from quantitative PCR analysis in the spinal cord showed that DILC was significantly up-regulated in rats with bCCI compared with the sham group. DILC down-regulation mediated by intrathecal administration of DILC siRNA significantly increased the mechanical shrinkage threshold (MWT) and paw withdrawal threshold latency (PWTL), decreased the positive frequency for nerve sensitivity to cold and suppressed the expression of inflammatory genes in bCCI rats. Down-regulation of DILC induced suppressor of cytokine signaling (SOCS3) expression and inhibited the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in spinal cord tissues. Western blotting showed that down-regulation of DILC by DILC siRNA transfection induced SOCS3 expression and inhibited the expression of p-Janus kinase 2 (p-JAK2) and p-STAT3 and their downstream genes in primary microglia. Furthermore, down-regulation of DILC increased the viability of primary microglia, suppressed apoptosis, and inhibited the production of interleukin (IL)-6 and IL-1β in microglia. In contrast, overexpression of DILC showed the opposite functions to those of DILC knockdown. In conclusion, silence of lncRNA DILC attenuates neuropathic pain via SOCS3-induced suppression of the JAK2/STAT3 pathway.
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Wang, Xiaoyang, Jie Zhao, Xiaochuan Wang, Jingjuan Zhang, Yi Wang, Xinyue Wang, Shanshan Jia, et al. "Bacterial cellulose membrane combined with BMSCs promotes wound healing by activating the notch signaling pathway." Frontiers in Surgery 9 (January 16, 2023). http://dx.doi.org/10.3389/fsurg.2022.1027067.

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ObjectiveThe bacterial cellulose membrane (BCM) has been widely studied and applied as a new biomaterial for wound healing, but causes pain with frequent dressing changes. Local application of bone marrow mesenchymal stem cells (BMSCs) requires a niche. Furthermore, the effect and mechanism of the BCM combined with BMSCs have not been reported.MethodsMorphological and chemical identifications of BCMs were investigated by porosity analyses, scanning electron microscopy, and Fourier-transform infrared spectroscopy. Biological wound dressings (BWDs) were prepared by the BCM in combination with BMSCs. The biological effects of BWDs on human dermal fibroblast (HDF) and VEGF-A in human vascular endothelial cells (HuVECs) were detected in vitro, and the effect of BWDs on acute wounds in mice was detected in vivo. Collagen and angiogenesis were evaluated through hematoxylin–eosin staining and Masson staining. The expressions of COL-1 and VEGF-A and the activation of the Notch signaling pathway in vivo and in vitro were detected by quantitative reverse-transcriptase polymerase chain reaction.ResultsThe BCM had a nanoscale structure and provided a partial niche for the survival and proliferation of BMSCs. BWDs were successfully prepared and regulated the biological behaviors of wound healing-related cells in vitro and upregulated the expressions of COL-1 in HDF and VEGF-A in HuVECs. BWDs promoted wound healing by increasing collagen type I synthesis and angiogenesis in acute wounds in mice.ConclusionsBWDs prepared by the combination of nanomaterial BCMs and BMSCs facilitated acute wound healing, which may be regulated by activating the Notch signaling pathway.
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Zhang, Wen-jun, Chen Luo, Chao Huang, Si-cheng Liu, and Hong-liang Luo. "Microencapsulated Neural Stem Cells Inhibit Sciatic Nerve Injury-Induced Pain by Reducing P2 × 4 Receptor Expression." Frontiers in Cell and Developmental Biology 9 (September 21, 2021). http://dx.doi.org/10.3389/fcell.2021.656780.

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Objectives: The purpose of this study is to investigate the effects of transplantation of microencapsulated neural stem cells (MC-NSCs), which downregulate the P2 × 4 receptor (P2 × 4R) overexpression and relieve neuropathic pain (NPP).Methods: Neural stem cells (NSCs) and MC-NSCs were transplanted to the injured sciatic nerve. Transmission electron microscope and immunofluorescence were used to observe the changes of injured sciatic nerve. Behavioral methods were used to detect mechanical withdrawal thresholds (MWT) and thermal withdrawal latency (TWL) of rats. Expression levels of P2 × 4Rs and p-p65 in the spinal cord segment of rats were measured by using molecular biology methods. The concentrations of IL-1β and TNF-α were detected in serum of rats by ELISA.Results: After sciatic nerve injury, the sciatic nerve fibers had the myelinated lamina separated, and disintegrated fragments could be seen. The fluorescence intensity of myelin MBP was weakened. The MWT and TWL were significantly decreased, the expression of P2 × 4Rs and p-p65 were significantly increased, and the concentrations of IL-1β and TNF-α were increased. After NSC and MC-NSC transplantation, the myelin sheath of the sciatic nerve was relatively intact, some demyelination changes could be seen, and the injured sciatic nerve has been improved. The fluorescence intensity of myelin MBP was increased. The MWT and TWL were increased, expression levels of P2 × 4Rs and p-p65 were decreased, and the concentrations of IL-1β and TNF-α were significantly decreased. Compared with NSC transplantation, transplantation of MC-NSCs could better repair the damaged sciatic nerve, decrease the expression of P2 × 4Rs and p-p65, decrease the level of IL-1β and TNF-α, and relieve pain (all p-values < 0.05).Conclusion: NSCs and MC-NSCs transplantation may alleviate pain by reducing the expression of P2 × 4Rs and inhibiting the activation of NF-KB signaling, while MC-NSCs transplantation has a better effect of suppressing pain. Our experimental results provide new data support for the treatment of NPP.
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Dissertations / Theses on the topic "Stem cells, VEGF signaling, Neuropathic pain"

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Vona, Alessia. "From rat adipose stem cells to VEGF signaling: emerging role for neuropathic pain relief." Doctoral thesis, 2020. http://hdl.handle.net/2158/1184459.

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Lo scopo del progetto di dottorato è stato quello di andare a cercare un link tra dolore neuropatico indotto da oxaliplatino, cellule staminali adipose di ratto e VEGF, andando a studiare un possibile meccanismo di azione attraverso il quale le cellule staminali riducono l'effetto pro-algesico del VEGF.
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Barbara, Tenci. "Effects of adipose derived stem cells in counteracting oxaliplatin-induced neuropathy: role of VEGF-A as possible applications." Doctoral thesis, 2018. http://hdl.handle.net/2158/1121434.

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Abstract:
Oxaliplatin therapy of colorectal cancer induces a dose-dependent neuropathic syndrome in 50% of patients. Pharmacological treatments may offer limited relief; scientific efforts are being solicited to define a new therapeutic approach. Interestingly, adult mesenchymal stem cells offer a totipotent cellular source for replacing injured neural cells and at the same time represent a source of neuroprotective and anti-inflammatory mediators, opposing the effect of nerve damage. In our hands, adipose-derived stem cells (ASCs) injection (2x106 ASCs/rat i.v.) were able to counteract mechanical hyperalgesia induced by repeated oxaliplatin administration in rats (2.4 mg kg-1 i.p. for a total of 10 administrations). This effect reached a maximum 6h after ASCs administration and lasted up to 72h. Subsequent ASCs administrations induced a reduction of hypersensitivity, with a similar efficacy trend over time. Investigating a possible mechanism of action by which ASCs exert their effect, 2x106 ASCs labeled with 1 µM of the fluorescent probe 5-(and-6-9-(((4-chloromethyl)benzoyl)amino) tetramethylrhodamine were injected in order to evaluate the localization of ASCs in the rat body. Labelled ASCs were detectable in the bloodstream 1 and 3 h after injection, the percentage gradually decreased, 24 h after administration no cells were found. At this time, ASCs were detected in the liver digested homogenate. No ASCs were found in the central nervous system and in lungs. VEGF-A, EGF and TGF-β were assayed in plasma. EGF and TGF-β were not altered by oxaliplatin or ASCs treatments. On the contrary, VEGF-A concentration significantly increased in oxaliplatin-treated rats in comparison to the control group whereas ASCs were able to counteract this alteration, suggesting both a possible implication of VEGF modulation in the development of neuropathic pain and in ASCs pain relieving mechanism. This hypothesis was strengthened by the reduction of oxaliplatin-induced hyperalgesia after an acute i.p. administration of the VEGF-antibody bevacizumab (dose-dependently, 1-15 mg kg-1). Moreover, plantar injection of the pain-related isoform VEGF165b (10-100 ng) in naïve rats, significantly decreased the pain threshold up to 3 h after administration in a bevacizumab-reverted manner (15 mg kg-1). VEGF165b (30-100 ng) dose-dependently, significantly reduced the weight tolerated on the posterior paw also after an intrathecal administration. These data led us to further investigate the role of VEGF-A in modulating pain signaling and the correlation between ASCs anti-nociceptive efficacy and VEGF-A modulation in central nervous system. As evaluated by western blot analysis, oxaliplatin repeated treatment significantly increased VEGF165b expression in spinal cord and PAG while in DRG, cortex and thalamus the protein levels were not influenced with respect to control group. ASCs i.v. injected significantly counteracted the oxaliplatin-dependent VEGF165b increase only in spinal cord. Accordingly, an intrathecal administration of ASCs (75x103/rat) was able to revert hyperalgesia induced by repeated oxaliplatin treatments starting from 1 h after the injection and up to 6 h. To further investigate the link between central VEGF-A and the modulation of pain perception, the selective neutralization of VEGF-A and VEGF165b was performed both in oxaliplatin-treated and in control rats. The specific antibody against VEGF165b, i.t. injected (7.5 μg/rat), significantly decrease oxaliplatin-induced hyperalgesia with similar efficacy to bevacizumab (45 μg/rat i.t. injected) but with higher potency. The modulation of VEGF-A is suggested as a key mechanism in the complex response orchestrated by stem cells against neuropathy and the role of ASCs “secretome” as effector of their efficacy is highlighted. For this reason, an artificial and biocompatible niche in which ASCs can be maintained was set up and the efficacy of this engineered niche in relieving oxaliplatin-induced neuropathic pain was tested. As physiologically occurs in tissues, the artificial niches should promote ASCs proliferation, ensuring the maintenance of their stemness and meanwhile permit a bidirectional flux of solutes from the inner and outer environment without a direct delivery of ASCs. For this purpose, 4x106 rASCs were encapsulated into each artificial niche (AlgiMatrix® sponge), the day after AlgiMatrix® sponges were implanted s.c. in the back of neuropathic rats (two sponges per rat). Encapsulated rASCs significantly reduced mechanical hypersensitivity induced by oxaliplatin treatment beginning 6h after the surgery. The effect on hypersensitivity remained constant for 7 days after AlgiMatrix® sponges implantation and disappeared at 8th day. Enclose ASCs in an artificial niche allows to exploit their modulatory capabilities in response to tissue injuries reducing possible side effects associated to stem cell differentiation. So, the present data suggest an alternative approach in the use of ASCs for the treatment of oxaliplatin-induced neuropathic pain.
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