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Relevant bibliographies by topics / GDNF

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Academic literature on the topic 'GDNF'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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Journal articles on the topic "GDNF"

1

Doretto, Lucas B., Arno J. Butzge, Rafael T. Nakajima, Emanuel R. M. Martinez, Beatriz Marques de Souza, Maira da Silva Rodrigues, Ivana F. Rosa, et al. "Gdnf Acts as a Germ Cell-Derived Growth Factor and Regulates the Zebrafish Germ Stem Cell Niche in Autocrine- and Paracrine-Dependent Manners." Cells 11, no. 8 (April 11, 2022): 1295. http://dx.doi.org/10.3390/cells11081295.

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Glial cell line-derived neurotrophic factor (GDNF) and its receptor (GDNF Family Receptor α1-GFRα1) are well known to mediate spermatogonial stem cell (SSC) proliferation and survival in mammalian testes. In nonmammalian species, Gdnf and Gfrα1 orthologs have been found but their functions remain poorly investigated in the testes. Considering this background, this study aimed to understand the roles of the Gdnf-Gfrα1 signaling pathway in zebrafish testes by combining in vivo, in silico and ex vivo approaches. Our analysis showed that zebrafish exhibit two paralogs for Gndf (gdnfa and gdnfb) and its receptor, Gfrα1 (gfrα1a and gfrα1b), in accordance with a teleost-specific third round of whole genome duplication. Expression analysis further revealed that both ligands and receptors were expressed in zebrafish adult testes. Subsequently, we demonstrated that gdnfa is expressed in the germ cells, while Gfrα1a/Gfrα1b was detected in early spermatogonia (mainly in types Aund and Adiff) and Sertoli cells. Functional ex vivo analysis showed that Gdnf promoted the creation of new available niches by stimulating the proliferation of both type Aund spermatogonia and their surrounding Sertoli cells but without changing pou5f3 mRNA levels. Strikingly, Gdnf also inhibited late spermatogonial differentiation, as shown by the decrease in type B spermatogonia and down-regulation of dazl in a co-treatment with Fsh. Altogether, our data revealed that a germ cell-derived factor is involved in maintaining germ cell stemness through the creation of new available niches, supporting the development of spermatogonial cysts and inhibiting late spermatogonial differentiation in autocrine- and paracrine-dependent manners.

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Moreau, Evelyne, José Vilar, Martine Lelièvre-Pégorier, Claudie Merlet-Bénichou, and Thierry Gilbert. "Regulation of c-ret expression by retinoic acid in rat metanephros: implication in nephron mass control." American Journal of Physiology-Renal Physiology 275, no. 6 (December 1, 1998): F938—F945. http://dx.doi.org/10.1152/ajprenal.1998.275.6.f938.

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Vitamin A and its derivatives have been shown to promote kidney development in vitro in a dose-dependent fashion. To address the molecular mechanisms by which all- trans-retinoic acid (RA) may regulate the nephron mass, rat kidneys were removed on embryonic day 14( E14) and grown in organ culture under standard or RA-stimulated conditions. By using RT-PCR, we studied the expression of the glial cell line-derived neurotrophic factor (GDNF), its cell surface receptor-α (GDNFR-α), and the receptor tyrosine kinase c-ret, known to play a major role in renal organogenesis. Expression of GDNF and GDNFR-α transcripts was high at the time of explantation and remained unaffected in culture with or without RA. In contrast, c-ret mRNA level, which was low in E14 metanephros and dropped rapidly in vitro, was increased by RA in a dose-dependent manner. The same is true at the protein level. Exogenous GDNF barely promotes additional nephron formation in vitro. Thus the present data establish c-ret as a key target of retinoids during kidney organogenesis.

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Marsh, Debbie J., Zimu Zheng, Andrew Arnold, Scott D. Andrew, Diana Learoyd, Andrea Frilling, Paul Komminoth, et al. "Mutation Analysis of Glial Cell Line-Derived Neurotrophic Factor, a Ligand for an RET/Coreceptor Complex, in Multiple Endocrine Neoplasia Type 2 and Sporadic Neuroendocrine Tumors." Journal of Clinical Endocrinology & Metabolism 82, no. 9 (September 1, 1997): 3025–28. http://dx.doi.org/10.1210/jcem.82.9.4197.

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Abstract Causative germline missense mutations in the RET proto-oncogene have been associated with over 92% of families with the inherited cancer syndrome multiple endocrine neoplasia type 2 (MEN 2). MEN 2A is characterized primarily by medullary thyroid carcinoma (MTC) and pheochromocytoma, both tumors of neural crest origin. Parathyroid hyperplasia or adenoma is also seen in MEN 2A, but rarely in MEN 2B, which has additional stigmata, including a marfanoid habitus, mucosal neuromas, and ganglioneuromatosis of the gastrointestinal tract. In familial MTC, MTC is the only lesion present. Somatic RET mutations have also been identified in a subset of sporadic MTCs, pheochromocytomas, and rarely, small cell lung cancer, but not in sporadic parathyroid hyperplasias/adenomas or other neuroendocrine tumors. Glial cell line-derived neurotrophic factor (GDNF) and its receptor molecule GDNFR-α, have recently been identified as members of the RET ligand binding complex. Therefore, the genes encoding both GDNF and GDNFR-α are excellent candidates for a role in the pathogenesis of those MEN 2 families and sporadic neuroendocrine tumors without RET mutations. No mutations were found in the coding region of GDNF in DNA samples from 9 RET mutation negative MEN 2 individuals (comprising 6 distinct families), 12 sporadic MTCs, 17 sporadic cases of parathyroid adenoma, and 10 small cell lung cancer cell lines. Therefore, we find no evidence that mutation within the coding regions of GDNF plays a role in the genesis of MEN 2 and sporadic neuroendocrine tumors.

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Walton, Kevin M. "GDNF." Molecular Neurobiology 19, no. 1 (February 1999): 43–59. http://dx.doi.org/10.1007/bf02741377.

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Tao, Le, Wenting Ma, Liu Wu, Mingyi Xu, Yanqin Yang, Wei Zhang, Wenjun Sha, et al. "Glial cell line-derived neurotrophic factor (GDNF) mediates hepatic stellate cell activation via ALK5/Smad signalling." Gut 68, no. 12 (June 6, 2019): 2214–27. http://dx.doi.org/10.1136/gutjnl-2018-317872.

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ObjectiveAlthough glial cell line-derived neurotrophic factor (GDNF) is a member of the transforming growth factor-β superfamily, its function in liver fibrosis has rarely been studied. Here, we investigated the role of GDNF in hepatic stellate cell (HSC) activation and liver fibrosis in humans and mice.DesignGDNF expression was examined in liver biopsies and sera from patients with liver fibrosis. The functional role of GDNF in liver fibrosis was examined in mice with adenoviral delivery of the GDNF gene, GDNF sgRNA CRISPR/Cas9 and the administration of GDNF-blocking antibodies. GDNF was examined on HSC activation using human and mouse primary HSCs. The binding of activin receptor-like kinase 5 (ALK5) to GDNF was determined using surface plasmon resonance (SPR), molecular docking, mutagenesis and co-immunoprecipitation.ResultsGDNF mRNA and protein levels are significantly upregulated in patients with stage F4 fibrosis. Serum GDNF content correlates positively with α-smooth muscle actin (α-SMA) and Col1A1 mRNA in human fibrotic livers. Mice with overexpressed GDNF display aggravated liver fibrosis, while mice with silenced GDNF expression or signalling inhibition by GDNF-blocking antibodies have reduced fibrosis and HSC activation. GDNF is confined mainly to HSCs and contributes to HSC activation through ALK5 at His39 and Asp76 and through downstream signalling via Smad2/3, but not through GDNF family receptor alpha-1 (GFRα1). GDNF, ALK5 and α-SMA colocalise in human and mouse HSCs, as demonstrated by confocal microscopy.ConclusionsGDNF promotes HSC activation and liver fibrosis through ALK5/Smad signalling. Inhibition of GDNF could be a novel therapeutic strategy to combat liver fibrosis.

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Shi, Haikun, Daniel Patschan, Gunnar P. H. Dietz, Mathias Bähr, Matthew Plotkin, and Michael S. Goligorsky. "Glial cell line-derived neurotrophic growth factor increases motility and survival of cultured mesenchymal stem cells and ameliorates acute kidney injury." American Journal of Physiology-Renal Physiology 294, no. 1 (January 2008): F229—F235. http://dx.doi.org/10.1152/ajprenal.00386.2007.

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Glial cell line-derived neurotrophic growth factor (GDNF), a member of the transforming growth factor family, is necessary for renal organogenesis and exhibits changes in expression in models of renal disease. Nestin is an intermediate filament protein originally believed to be a marker of neuroepithelial stem cells and recently proposed as a marker of mesenchymal stem cells (MSC). Having demonstrated the participation of nestin-expressing cells in renoprotection during acute renal ischemia, we hypothesized that growth factors and transcription factors similar to those operating in the nervous system should be also operant in the kidney and may be induced after noxious stimuli, such as an ischemic episode. Using cultured kidney-derived MSC, which abundantly express nestin, we confirmed expression of GDNF by these cells and demonstrated the GDNF-induced expression of GDNF. The cellular expression of nestin paralleled that of GDNF: serum starvation decreased the expression, whereas application of GDNF resulted in a dose-dependent increase in nestin expression. Immunohistochemical and Western blot analyses of kidneys obtained from control and postischemic mice showed that expression of GDNF was much enhanced in the renal cortex, a pattern similar to the previously reported expression of nestin. Based on the observed GDNF-induced GDNF expression, we next explored the effect of supplemental GDNF administered early after ischemia on renal function postischemia. GDNF-treated mice were protected against acute ischemia. To address potential mechanisms of the observed renoprotection, in vitro studies showed that GDNF accelerated MSC migration in a wound-healing assay. Hypoxia did not accelerate, but rather slightly reduced, the motility of MSC and reduced the expression of GDNF in MSC by approximately twofold. Furthermore, GDNF was cytoprotective against oxidative stress-induced apoptotic death of MSC. Collectively, these data establish 1) an autoregulatory circuit of GDNF-induced GDNF expression in renal MSC; 2) induction of GDNF expression in postischemic kidneys; 3) the ability of exogenous GDNF to ameliorate ischemic renal injury; and 4) a possible contribution of GDNF-induced motility and improved survival of MSC to renoprotection.

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Magill, Christina K., Amy M. Moore, Ying Yan, Alice Y. Tong, Matthew R. MacEwan, Andrew Yee, Ayato Hayashi, et al. "The differential effects of pathway- versus target-derived glial cell line–derived neurotrophic factor on peripheral nerve regeneration." Journal of Neurosurgery 113, no. 1 (July 2010): 102–9. http://dx.doi.org/10.3171/2009.10.jns091092.

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Object Glial cell line–derived neurotrophic factor (GDNF) has potent survival effects on central and peripheral nerve populations. The authors examined the differential effects of GDNF following either a sciatic nerve crush injury in mice that overexpressed GDNF in the central or peripheral nervous systems (glial fibrillary acidic protein [GFAP]–GDNF) or in the muscle target (Myo-GDNF). Methods Adult mice (GFAP-GDNF, Myo-GDNF, or wild-type [WT] animals) underwent sciatic nerve crush and were evaluated using histomorphometry and muscle force and power testing. Uninjured WT animals served as controls. Results In the sciatic nerve crush, the Myo-GDNF mice demonstrated a higher number of nerve fibers, fiber density, and nerve percentage (p < 0.05) at 2 weeks. The early regenerative response did not result in superlative functional recovery. At 3 weeks, GFAP-GDNF animals exhibit fewer nerve fibers, decreased fiber width, and decreased nerve percentage compared with WT and Myo-GDNF mice (p < 0.05). By 6 weeks, there were no significant differences between groups. Conclusions Peripheral delivery of GDNF resulted in earlier regeneration following sciatic nerve crush injuries than that with central GDNF delivery. Treatment with neurotrophic factors such as GDNF may offer new possibilities for the treatment of peripheral nerve injury.

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Popsueva, Anna, Dmitry Poteryaev, Elena Arighi, Xiaojuan Meng, Alexandre Angers-Loustau, David Kaplan, Mart Saarma, and Hannu Sariola. "GDNF promotes tubulogenesis of GFRα1-expressing MDCK cells by Src-mediated phosphorylation of Met receptor tyrosine kinase." Journal of Cell Biology 161, no. 1 (April 7, 2003): 119–29. http://dx.doi.org/10.1083/jcb.200212174.

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Glial cell line–derived neurotrophic factor (GDNF) and hepatocyte growth factor (HGF) are multifunctional signaling molecules in embryogenesis. HGF binds to and activates Met receptor tyrosine kinase. The signaling receptor complex for GDNF typically includes both GDNF family receptor α1 (GFRα1) and Ret receptor tyrosine kinase. GDNF can also signal independently of Ret via GFRα1, although the mechanism has remained unclear. We now show that GDNF partially restores ureteric branching morphogenesis in ret-deficient mice with severe renal hypodysplasia. The mechanism of Ret-independent effect of GDNF was therefore studied by the MDCK cell model. In MDCK cells expressing GFRα1 but no Ret, GDNF stimulates branching but not chemotactic migration, whereas both branching and chemotaxis are promoted by GDNF in the cells coexpressing Ret and GFRα1, mimicking HGF/Met responses in wild-type MDCK cells. Indeed, GDNF induces Met phosphorylation in several ret-deficient/GFRα1-positive and GFRα1/Ret-coexpressing cell lines. However, GDNF does not immunoprecipite Met, making a direct interaction between GDNF and Met highly improbable. Met activation is mediated by Src family kinases. The GDNF-induced branching of MDCK cells requires Src activation, whereas the HGF-induced branching does not. Our data show a mechanism for the GDNF-induced branching morphogenesis in non-Ret signaling.

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Cintrón-Colón, Alberto F., Gabriel Almeida-Alves, Alicia M. Boynton, and John M. Spitsbergen. "GDNF synthesis, signaling, and retrograde transport in motor neurons." Cell and Tissue Research 382, no. 1 (September 8, 2020): 47–56. http://dx.doi.org/10.1007/s00441-020-03287-6.

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Abstract Glial cell line–derived neurotrophic factor (GDNF) is a 134 amino acid protein belonging in the GDNF family ligands (GFLs). GDNF was originally isolated from rat glial cell lines and identified as a neurotrophic factor with the ability to promote dopamine uptake within midbrain dopaminergic neurons. Since its discovery, the potential neuroprotective effects of GDNF have been researched extensively, and the effect of GDNF on motor neurons will be discussed herein. Similar to other members of the TGF-β superfamily, GDNF is first synthesized as a precursor protein (pro-GDNF). After a series of protein cleavage and processing, the 211 amino acid pro-GDNF is finally converted into the active and mature form of GDNF. GDNF has the ability to trigger receptor tyrosine kinase RET phosphorylation, whose downstream effects have been found to promote neuronal health and survival. The binding of GDNF to its receptors triggers several intracellular signaling pathways which play roles in promoting the development, survival, and maintenance of neuron-neuron and neuron-target tissue interactions. The synthesis and regulation of GDNF have been shown to be altered in many diseases, aging, exercise, and addiction. The neuroprotective effects of GDNF may be used to develop treatments and therapies to ameliorate neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). In this review, we provide a detailed discussion of the general roles of GDNF and its production, delivery, secretion, and neuroprotective effects on motor neurons within the mammalian neuromuscular system.

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Zaman, V., Z. Li, L. Middaugh, S. Ramamoorthy, B. Rohrer, M. E. Nelson, A. C. Tomac, B. J. Hoffer, G. A. Gerhardt, and A. Ch Granholm. "The Noradrenergic System of Aged GDNF Heterozygous Mice." Cell Transplantation 12, no. 3 (April 2003): 291–303. http://dx.doi.org/10.3727/000000003108746740.

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Glial cell line-derived neurotrophic factor (GDNF) is a trophic factor for noradrenergic (NE) neurons of the pontine nucleus locus coeruleus (LC). Decreased function of the LC-NE neurons has been found during normal aging and in neurodegenerative disorders. We have previously shown that GDNF participates in the differentiation of LC-NE neurons during development. However, the continued role of GDNF for LC-NE neurons during maturation and aging has not been addressed. We examined alterations in aged mice that were heterozygous for the GDNF gene (Gdnf+/–). Wild-type (Gdnf+/+) and Gdnf+/– mice (18 months old) were tested for locomotor activity and brain tissues were collected for measuring norepinephrine levels and uptake, as well as for morphological analysis. Spontaneous locomotion was reduced in Gdnf+/– mice in comparison with Gdnf+/+ mice. The reduced locomotor activity of Gdnf +/– mice was accompanied by reductions in NE transporter activity in the cerebellum and brain stem as well as decreased norepinephrine tissue levels in the LC. Tyrosine hydroxylase (TH) immunostaining demonstrated morphological alterations of LC-NE cell bodies and abnormal TH-positive fibers in the hippocampus, cerebellum, and frontal cortex of Gdnf+/– mice. These findings suggest that the LC-NE system of Gdnf+/– mice is impaired and suggest that GDNF plays an important role in continued maintenance of this neuronal system throughout life.

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More sources

Dissertations / Theses on the topic "GDNF"

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Ivanchuk, Stacey M. "Expression of RET, GDNF and GDNFR-Ã in human development and disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq20655.pdf.

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DHALIWAL, PARVIN. "PARKINSON'S GDNF THERAPY AND OXIDATIVE STRESS." Thesis, The University of Arizona, 2008. http://hdl.handle.net/10150/190438.

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Roxo, Tiago Filipe Dias Santos. "Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?" Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1625.

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Microglia are the resident macrophages of the Central Nervous System and act as the main form of immune defence. Microglia can assume an activated state in case of inflammation, having its phagocytic activity increased, also releasing reactive oxygen species, in order to protect the Central Nervous System cells from injury. However, activated microglia has also been associated with neurodegeneration. Increased interleukin and cytokine levels have been described in neurodegenerative diseases, namely Parkinson’s disease, where the loss of dopaminergic neurons has been related to excessive microglial activation. Soluble factors released by astrocytes are capable to modulate microglial reactivity. From these factors, glial cell line-derived neurotrophic factor (GDNF) stood out for its ability to protect dopaminergic neurons from injury, both in vitro an in vivo. Some studies have also demonstrated an anti-inflammatory action of GDNF, mediated by its receptor GFR1, suggesting that these two effects of GDNF may be related to each other. However, no study has provided a clear evidence for a cause-effect relationship between them. Therefore, this work aims at elucidating the importance of GDNF control of microglial reactivity to the survival of dopaminergic neurons. The main strategy will be to block the action of GDNF specifically in microglial cells, through GFR1 silencing, and to evaluate its effect on the neuroprotective action of GDNF in the presence of an inflammatory stimuli. The expression of GFR1 in primary ventral midbrain microglia and N9 microglia cell line cultures was confirmed through immunochemistry and Western Blot. Silencing of GFR1, through siRNA, in N9 microglia cells was successfully accomplished and preliminary results suggest that silencing of this receptor in primary cultures of microglia is also doable. Co-cultures of N9 microglia cells and neuron-glia mixed cultures were exposed to different concentrations of LPS which induced a selective dopaminergic injury. Under these conditions, an increase in microglial reactivity was observed. Additional experiments will be necessary to achieve the main goal of this work. However, these results will support future experiments in order to elucidate the relevance of the anti-inflammatory effect of GDNF on dopaminergic neuroprotection.
As microglias são os macrófagos residentes do Sistema Nervoso Central e actuam como a principal forma de defesa imunitária. Podem assumir um estado denominado activado, tendo a sua capacidade fagocítica aumentada e produzindo espécies reactivas de oxigénio, com o propósito de proteger as células do Sistema Nervoso Central. No entanto, este estado activado tem sido também relacionado com um processo neurodegenerativo. Aumentos dos níveis de interleucinas e citocinas têm sido descritos em doenças neurodegenerativas, nomeadamente na doença de Parkinson, onde a perda de neurónios dopaminérgicos tem sido associada a uma excessiva activação microglial. Factores solúveis libertados pelos astrócitos mostraram ser capazes de modular a reactividade microglial. Destes factores, o factor derivado de uma linha de células da glia (GDNF) destacou-se pela sua capacidade em proteger os neurónios dopaminérgicos, tanto in vitro como in vivo. Alguns estudos têm também demonstrado uma acção anti-inflamatória do GDNF, mediada pelo receptor GFR1, sugerindo que possa existir uma relação entre estes dois efeitos. No entanto, até ao momento, não foi ainda demonstrada uma relação de causaefeito entre eles. Assim, este trabalho tem como objectivo elucidar a importância do controlo da reactividade microglial pelo GDNF na sobrevivência dos neurónios dopaminérgicos. A estratégia principal será impedir a acção do GDNF especificamente na microglia, através do silenciamento do receptor GFR1, e avaliar o efeito deste silenciamento na acção neuroprotectora do GDNF após aplicação de um estímulo inflamatório. A expressão de GFR1 em culturas primárias de microglia do mesencéfalo ventral e numa linha celular de microglia N9 foi confirmada por imunocitoquímica e Western Blot. O silenciamento do receptor GFR1 na linha celular de microglia N9 foi alcançado com sucesso e resultados preliminares sugerem que o silenciamento deste receptor em culturas primárias de microglia é também possível. A exposição de co-culturas de microglia N9 e culturas mistas de neurónios e glia do mesencéfalo ventral a diferentes concentrações de LPS induziu a morte selectiva de neurónios dopaminérgicos. Paralelamente, foi possível observar um aumento da reactividade microglial. Experiências adicionais serão necessárias para atingir o objectivo principal deste trabalho. No entanto, estes resultados servirão de base para, em futuras experiências, elucidar a relevância do efeito anti-inflamatório do GDNF na neuroprotecção dopaminérgica.

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Trupp, Miles. "Neurotrophic signalling by GDNF and its receptors /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980602trup.

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Fink, Erin Nicole. "GM1 signaling through the GDNF receptor complex." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1198013799.

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Chermenina, Maria. "GDNF and alpha-synuclein in nigrostriatal degeneration." Doctoral thesis, Umeå universitet, Histologi med cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-91811.

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Parkinson’s disease is a common neurological disorder with a complex etiology. The disease is characterized by a progressive loss of dopaminergic cells in the substantia nigra, which leads to motor function and sometimes cognitive function disabilities. One of the pathological hallmarks in Parkinson’s disease is the cytoplasmic inclusions called Lewy bodies found in the dopamine neurons. The aggregated protein α-synuclein is a main component of Lewy bodies. In view of severe symptoms and the upcoming of problematic side effects that are developed by the current most commonly used treatment in Parkinson’s disease, new treatment strategies need to be elucidated. One such strategy is replacing the lost dopamine neurons with new dopamine-rich tissue. To improve survival of the implanted neurons, neurotrophic factors have been used. Glial cell line-derived neurotrophic factor (GDNF), which was discovered in 1993, improves survival of ventral mesencephalic dopamine neurons and enhances dopamine nerve fiber formation according to several studies. Thus, GDNF can be used to improve dopamine-rich graft outgrowth into the host brain as well as inducing sprouting from endogenous remaining nerve fibers. This study was performed on Gdnf gene-deleted mice to investigate the role of GDNF on the nigrostriatal dopamine system. The transplantation technique was used to create a nigrostriatal microcircuit from ventral mesencephalon (VM) and the lateral ganglionic eminence (LGE) from different Gdnf gene-deleted mice. The tissue was grafted into the lateral ventricle of wildtype mice. The results revealed that reduced concentrations of GDNF, as a consequence from the Gdnf gene deletion, had effects on survival of dopamine neurons and the dopamine innervation of the nigrostriatal microcircuit. All transplants had survived at 3 months independently of Gdnf genotype, however, the grafts derived from Gdnf gene-deleted tissue had died at 6 months. Transplants with partial Gdnf gene deletion survived up to 12 months after transplantation. Moreover, the dopaminergic innervation of striatal co-grafts was impaired in Gdnf gene-deleted tissue. These results highlight the role of GDNF for long-term maintenance of the nigrostriatal dopamine system. To further investigate the role of GDNF expression on survival and organization of the nigrostriatal dopamine system, VM and LGE as single or combined to double co-grafts created from mismatches in Gdnf genotypes were transplanted into the lateral ventricle of wildtype mice. Survival of the single grafts was monitored over one year using a 9.4T MR scanner. The size of single LGE transplants was significantly reduced by the lack of GDNF already at 2 weeks postgrafting while the size of single VM was maintained over time, independently of GDNF expression. The double grafts were evaluated at 2 months, and the results revealed that lack of GDNF in LGE reduced the dopamine cell survival, while no loss of dopamine neurons was found in VM single grafts. The dopaminergic innervation of LGE was affected by absence of GDNF, which also caused a disorganization of the striatal portion of the co-grafts. Small, cytoplasmic inclusions were frequently found in the dopamine neurons in grafts lacking GDNF expression. These inclusions were not possible to classify as Lewy bodies by immunohistochemistry and the presence of phospho-α-synuclein and ubiquitin; however, mitochondrial dysfunction could not be excluded. To further study the death of the dopamine neurons by the deprivation of GDNF, the attention was turned to how Lewy bodies are developed. With respect to the high levels of α-synuclein that was found in the striatum, this area was selected as a target to inject the small molecule – FN075, which stimulates α-synuclein aggregation, to further investigate the role of α-synuclein in the formation of cytoplasmic inclusions. The results revealed that cytoplasmic inclusions, similar to those found in the grafts, was present at 1 month after the injection, while impairment in sensorimotor function was exhibited, the number of dopamine neurons was not changed at 6 months after the injection. Injecting the templator to the substantia nigra, however, significantly reduced the number of TH-positive neurons at 3 months after injection. In conclusion, these studies elucidate the role of GDNF for maintenance and survival of the nigrostriatal dopamine system and mechanisms of dopamine cell death using small molecules that template the α-synuclein aggregation.

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Oliveira, Julieta Conceição Mendes Borges. "GDNF e GPER: novas ferramentas no controlo da neuroinflamação?" Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1628.

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As células microgliais, os macrófagos residentes no sistema nervoso central, são responsáveis pela resposta imune inata. Quando são moderadamente ativadas, realizam funções vitais, fagocitando células mortas e removendo detritos celulares e toxinas. No entanto, uma ativação persistente destas células pode resultar numa desregulação da sua atividade. Elas podem tornar-se reativas e contribuir para a morte neuronal. Evidências crescentes sugerem que a inflamação e o stress oxidativo mediado pela microglia reativa desempenham um papel fundamental na progressão de várias doenças neurodegenerativas, como a doença de Parkinson. Tanto o fator neurotrófico derivado de uma linha de células da glia (GDNF) como os estrogénios são relatados por atuar na microglia, controlando a sua ativação excessiva. Um estudo anterior do nosso grupo mostrou que o GDNF presente em meio condicionado de astrócitos consegue inibir a reatividade microglial induzida pelo Zymozan A numa cultura primária de microglia do mesencéfalo ventral. O primeiro objetivo do presente trabalho foi o de verificar se a presença de neurónios, lesados ou não, poderia influenciar este efeito anti-inflamatório exercido pelo GDNF. Utilizando o mesmo tipo de cultura verificámos que o condicionamento na presença de neurónios reverteu a inibição da produção de NO exercida pelos meios condicionados apenas por astrócitos na microglia estimulada com LPS. Este diferente efeito dos dois meios poderá estar relacionado com o facto de os meios condicionados por culturas mistas de neurónios e astrócitos apresentaram níveis mais baixos de GDNF que os meios condicionados apenas por astrócitos. Por outro lado, estudos utilizando culturas primárias de microglia, bem como linhas celulares, demonstraram a capacidade do estrogénio para atenuar a ativação da microglia, em termos de atividade fagocítica, produção de espécies reativas de oxigénio e de azoto, bem como de outros fatores da cascata inflamatória. Está já descrita a capacidade dos estrogénios ativarem os recetores de estrogénio α e β presentes na microglia. No entanto, mais recentemente identificou-se um recetor de estrogénios transmembranar, o recetor de estrogénio acoplado à proteína G (GPER). O segundo objetivo do trabalho foi esclarecer a participação do GPER no controle da reatividade microglial mediada pelo estradiol. Utilizando uma linha celular de microglia N9, um agonista e um antagonista seletivos do recetor, verificamos que a ativação do GPER promoveu a migração das células microgliais e reduziu significativamente os parâmetros de reatividade microglial estudados. Estes resultados sugerem que o GPER pode ser um importante alvo terapêutico para doenças neurodegenerativas e neuroinflamatórias, especialmente nos homens, nos quais a terapia com estrogénio não é viável.
Microglial cells, the macrophages resident in the central nervous system, are responsible for the innate immune response. When moderately activated, these cells perform vital functions such as phagocytosing dead cells and removing cell debris and toxins. However, a persistent activation of these cells may result in deregulation of its activity. They can become reactive and contribute to neuronal death. Increasing evidences suggests that inflammation and oxidative stress mediated by reactive microglia play a key role in the progression of various neurodegenerative diseases such as Parkinson's disease. Both the glial cell line derived neurotrophic factor (GDNF) and estrogens are reported to play a role in this process and to control excessive activation of microglia. A previous study from our group that used a primary culture of ventral midbrain microglia showed that GDNF present in medium conditioned by astrocytes can inhibit microglial reactivity induced by Zymozan A. The first objective of the present study was to verify if the presence of neurons, injured or not, could influence this anti-inflammatory effect exerted by GDNF. Using the same culture we found that media conditioned by both astrocytes and neurons was no longer capable of inhibiting NO production on LPS-stimulated microglia. The different effects of the two media may be related to the fact that the media conditioned by cultures of neurons and astrocytes presented lower levels of GDNF as compared with media conditioned only by astrocytes. On the other hand, studies using primary cultures and microglia cell lines demonstrated the ability of estrogen to attenuate parameters of microglial activation such as phagocytic activity, production of reactive oxygen and nitrogen, as well as other factors inflammatory cascade. The ability of estrogens to regulate estrogen receptors α and β present in microglia was previously described. However, more recently a transmembrane estrogen receptor, the G-protein coupled estrogen receptor (GPER) was identified. The objective of the second part of the present work was to clarify the involvement of GPER in the control microglial reactivity mediated by estradiol. Using the N9 microglial cell line, an agonist and an antagonist of GPER receptor, we found that GPER activation promoted the migration of microglial cells and significantly reduced the various parameters of microglial reactivity evaluated. Taken together these results suggest that GPER can be an important therapeutic target for neurodegenerative and neuroinflammatory diseases, especially in males, for whom estrogen therapy is not feasible.

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Fonseca, Ana Paula da Silva. "Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio." Master's thesis, Universidade da Beira Interior, 2010. http://hdl.handle.net/10400.6/799.

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Abstract:

A doença de Parkinson é a segunda doença neurodegenerativa mais comum, depois do Alzheimer, e caracteriza-se principalmente pela perda progressiva de neurónios dopaminérgicos na Substantia Nigra. Numerosos trabalhos reportaram a maior prevalência e incidência desta doença no sexo masculino, relativamente ao sexo feminino. Estudos envolvendo a reposição com estrogénios em ratos fêmea ovariectomizados, atribuíram esta diferença de incidências ao efeito neuroprotectivo do estrogénio. No entanto, o grau de protecção exercida por níveis fisiológicos desta hormona permanece desconhecido. Os estrogénios também têm sido implicados na regulação da expressão de factores neurotróficos, o que pode estar na origem dos seus efeitos neuroprotectores. O factor neurotrófico derivado de uma linha de células da glia (GDNF) é um dos factores neurotróficos regulados pelo estrogénio, que foi implicado na neuroprotecção e regeneração na via nigroestriatal, actuando como um potente factor de sobrevivência para os neurónios dopaminérgicos, que são alvo de degeneração na doença de Parkinson. De forma a esclarecer o papel dos níveis endógenos de estrogénio na protecção da via nigroestriatal, utilizámos como modelo da doença de Parkinson a 6-hidroxidopamina, e estudámos de que forma a remoção dos ovários em fêmeas férteis interferiu com a extenção da lesão dopaminérgica induzida pela toxina. As fêmeas Wistar foram ovariectomizadas e 3 semanas após a cirurgia os animais foram injectados estereotaxicamente, no estriado, com 6-hidroxidopamina. A extensão da lesão foi avaliada através da contagem de células que expressavam o marcador dopaminérgico tirosina hidroxilase, por imunohistoquimica, assim como pelos níveis de expressão desta proteína, por western blot, tanto na Substantia Nigra como no estriado. Os níveis plasmáticos de estradiol também foram quantificados. De forma a determinar a a existência de relação entre os níveis de estradiol, a expressão de GDNF e a extensão da lesão dopaminérgica, também foi estudada a expressão do factor neurotrófico GDNF. Os nossos resultados sugerem fortemente que o estrogénio produzido endogenamente, assim como o GDNF, estão associados com níveis aumentados de tirosina hidroxilase estriatal, um marcador de sobrevivência da célula dopaminérgica.
Parkinson´s disease is the second most common neurodegenerative disorder after Alzheimer and is mainly characterized by a progressive and selective depletion of dopamine neurons in the Substantia Nigra. Numerous studies have reported a greater prevalence and incidence of PD in men than in women. Studies involving estrogen treatment of ovariectomised rodents attribute this largely to the neuroprotective effets of estrogen. However, a neuroprotective role for physiologic levels of circulating estrogen in females is less clear. Estrogens have also been shown to regulate the expression of neurotrophic factors, like glial cell line-derived neurotrophic factor (GDNF), which might mediate their neuroprotective effects. GDNF produces neuroprotective and regenerative effects in the nigrostriatal pathways, acting as a potent survival factor for dopaminergic neurons that degenerate in Parkinson’s disease. In order to clarify the role of endogenous levels of estrogens in protecting the nigrostriatal pathway, we used the 6-hydroxydopamine (6-OHDA) model of Parkinson’s disease and tested how the removal of ovaries in fertile females interferes with extent of the dopaminergic lesion induced by 6-OHDA. Female Wistar rats were ovariectomised and 3 weeks after the surgery the animals were stereotaxically injected in the striatum with 6-OHDA. The extent of the lesion was assessed by counting the cells expressing the dopaminergic marker tyrosine hydroxylase by imunohistochemistry and also the expression levels of this protein by Western blot in both the Substantia Nigra and the striatum. The plasma levels of estradiol were also quantified. To determine if there was a relationship between estradiol levels, the expression of GDNF and the extent of the dopaminergic lesion, we also studied the expression of the neurotrophic factor GDNF. Our findings strongly suggest that endogenously produced estrogens and GDNF are associated with increased levels of striatal tyrosine hydroxylase, a marker of dopaminergic cell survival.

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Wartiovaara, Kirmo. "GDNF and p75 neurotrophin receptor in development and disease." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/biola/vk/wartiovaara/.

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Åkerud, Peter. "GDNF family ligands and neural stem cells in Parkinson's disease /." Stockholm : [Karolinska Univ. Press], 2001. http://diss.kib.ki.se/2001/91-7349-042-3/.

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Books on the topic "GDNF"

1

David, Dellafiora, and Saltram House, eds. GDN PL7. [Plympton?]: National Trust, 1991.

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Decèze, Dominique. Haute tension à EDF-GDF. Paris: Gawsewitch, 2005.

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Universitas Indonesia. Pusat Penelitian Pranata Pembangunan., ed. Evaluasi pelaksanaan GDN di DKI Jakarta. [Jakarta]: Kerja sama Pusat Penelitian Pranata Pembangunan, UI dengan Direktorat Sosial Politik, DKI Jakarta, 1997.

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Pierre-Eric, Tixier, and Mauchamp Nelly, eds. EDF-GDF: Une entreprise publique en mutation. Paris: La Découverte, 2000.

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Weber, Uwe. Der Grenzüberschreitende Datenfluss (GDF): Ein neues Phänomen der internationalen Kommunikation. München: R. Fischer, 1993.

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GDF-Suez, Arcelor, EADS, Pechiney: Les dossiers noirs de la droite. Paris: Gawsewitch, 2007.

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McPhee, Jennifer. ID-1 and GDF-8 as negative regulators of skeletal muscle mass. Sudbury, Ont: Laurentian University, Behavioural Neuroscience Program, 1998.

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Marcel, Goldberg, Leclerc Annette, and Bugel Isabelle, eds. Cohorte GAZEL, 20000 volontaires d'EDF-GDF pour la recherche médicale: Bilan 1989-1993. Paris: Editions INSERM, 1994.

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Germany) Group Decision and Negotiation (Conference) (7th 2006 Karlsruhe. Group Decision and Negotiation (GDN) 2006: International conference, Karlsruhe, Germany, June 25-28, 2006 : proceedings. Edited by Seifert Stefan 1971 editor and Weinhardt Christof editor. Karlsruhe: Universitätsverlag Karlsruhe, 2006.

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Condijts, Joan. GDF-Suez, le dossier secret de la fusion: Enquête dans les coulisses du capitalisme à la française. Paris: Michalon, 2008.

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Book chapters on the topic "GDNF"

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Peterziel, H., and J. Strelau. "GDNF and Related Proteins." In Handbook of Neurochemistry and Molecular Neurobiology, 69–91. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-30381-9_4.

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Kiuchi, K., and H. Xiao. "GDNF-Induced Expression of Tyrosine Hydroxylase." In Catecholamine Research, 115–18. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3538-3_24.

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Rossi, Jari, and Matti S. Airaksinen. "GDNF Family Signalling in Exocrine Tissues: Distinct Roles for GDNF and Neurturin in Parasympathetic Neuron Development." In Advances in Experimental Medicine and Biology, 19–26. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0717-8_2.

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Unsicker, K., C. Suter-Crazzolara, and K. Krieglstein. "Neurotrophic Roles of GDNF and Related Factors." In Neurotrophic Factors, 189–224. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59920-0_8.

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Rosenblad, Carl, Deniz Kirik, and Anders Björklund. "Effects of GDNF on Nigrostriatal Dopamine Neurons." In Advances in Behavioral Biology, 117–30. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0179-4_12.

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Bankiewicz, Krystof, Waldy San Sebastian, Lluis Samaranch, and John Forsayeth. "GDNF and AADC Gene Therapy for Parkinson’s Disease." In Translational Neuroscience, 65–88. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4899-7654-3_4.

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Barua, Sonia, and Yashwant V. Pathak. "Unilateral Ex Vivo Gene Therapy by GDNF in Neurodegenerative Diseases." In Gene Delivery Systems, 155–61. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003186069-9.

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Sariola, Hannu, and Tiina Immonen. "GDNF Maintains Mouse Spermatogonial Stem Cells In Vivo and In Vitro." In Methods in Molecular Biology™, 127–35. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-214-8_9.

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Nitta, Atsumi, Rina Murai, Keiko Maruyama, and Shoei Furukawa. "FK506 Protects Dopaminergic Degeneration Through Induction of GDNF in Rodent Brains." In Mapping the Progress of Alzheimer’s and Parkinson’s Disease, 463–67. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-0-306-47593-1_79.

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Cass, Wayne A., Cecilia M. Kearns, and Don M. Gash. "Protective and Regenerative Properties of GDNF in the Central Nervous System." In Neuroprotective Signal Transduction, 145–61. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-475-7_8.

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Conference papers on the topic "GDNF"

1

Torres Ortega, Pablo Vicente, Cristian Smerdou, Elisa Garbayo, and María J. Blanco Prieto. "Sustained GDNF delivery via PLGA nanoparticles." In The 1st International Electronic Conference on Pharmaceutics. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/iecp2020-08799.

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Marquardt, Laura M., and Shelly E. Sakiyama-Elbert. "Effect of GDNF on schwann cell differentiation and interaction with neurons in vitro." In 2014 40th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2014. http://dx.doi.org/10.1109/nebec.2014.6972867.

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Feng, R., L. Tao, W. Ma, L. Wu, E. Seki, C. Liu, and S. Dooley. "Glial cell line-derived neurotrophic factor (GDNF) mediates hepatic stellate cell activation via ALK5/Smad signaling." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695260.

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Bhoj, Vijay G., Selene Nunez-Cruz, Kenneth Zhou, Dimitrios Arhontoulis, Michael Feldman, Keith Mansfield, Haiyong Peng, Christoph Rader, Don L. Siegel, and Michael C. Milone. "Abstract 2295: GDNF family receptor alpha 4 (GFRa4)-targeted adoptive T-cell immunotherapy for medullary thyroid carcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2295.

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Ferrante, Catherine A., Nikki DeAngelis, and Raluca Verona. "Abstract 4048: GFRα1 is required for GDNF-induced viability, migration, and signaling through RET in breast cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4048.

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Gardaneh, Mossa, and Sahar Shojaei. "Abstract 969: The anti-apoptotic impact of neurotrophic factor GDNF on breast cancer cells pre-treated with trastuzumab." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-969.

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Fan, Ching-Hsiang, Chien-Yu Ting, En-Ling Chang, Hao-Li Liu, Hong-Lin Chan, You-Yin Chen, and Chih-Kuang Yeh. "Ultrasound-triggered and targeted gene delivery by using cationic microbubbles to enhance GDNF gene transfection in a rat Parkinson's disease model." In 2015 IEEE International Ultrasonics Symposium (IUS). IEEE, 2015. http://dx.doi.org/10.1109/ultsym.2015.0204.

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Morandi, Andrea, Lesley-Ann Martin, Qiong Gao, Alan Mackay, David Robertson, Marketa Zvelebil, Mitch Dowsett, Ivan Plaza-Menacho, and Clare M. Isacke. "Abstract 4761: Glial cell derived neurotrophic factor (GDNF)-RET signaling as a target in aromatase inhibitor resistant ER-positive breast cancers." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4761.

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Asker, Hasan. "The Effects of Cinnamon Extract Supplementation on Immunolocalization of Glial Cell Line Derived Neurotrophic Factor (GDNF) in Testis of Diabetic Rats." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-89.

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Cavel, Oren, Richard J. Wong, Olga Shomron, Moran Amit, and Ziv Gil. "Abstract 1529: Endoneurial macrophages induce perineural invasion of pancreatic cancer cells by secretion of GDNF and activation of RET tyrosine kinase receptor." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1529.

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Reports on the topic "GDNF"

1

Svendsen, Clive N. Regulated GDNF Delivery In Vivo using Neural Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436921.

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Svendsen, Clive N. Regulated GDNF Delivery in Vivo Using Neural Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada428919.

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Svendsen, Clive. Regulated GDNF Delivery in Vivo Using Neural Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada471929.

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Svendsen, Clive, and Genevieve Gowing. Muscle-Derived GDNF: A Gene Therapeutic Approach for Preserving Motor Neuron Function in ALS. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada621394.

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Hoke, Ahmet, and Hai-Quan Mao. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada613645.

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Hoke, Ahmet, and Hai-Quan Mao. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581474.

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Christe, Kari. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599060.

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Christe, Kari, Leif Havton, and Ahmet Hoke. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Non-Human Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581480.

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Blanchat, Thomas K., Patrick Dennis Brady, Dann A. Jernigan, Anay Josephine Luketa, Mark R. Nissen, Carlos Lopez, Nancy Vermillion, and Marion Michael Hightower. Cost estimate for a proposed GDF Suez LNG testing program. Office of Scientific and Technical Information (OSTI), February 2014. http://dx.doi.org/10.2172/1204098.

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Zhou, Zhongwei, Hongli Liu, Huixiang Ju, Hongmei Chen, Li Li, Hao Jin, and Mingzhong Sun. Circulating GDF-15 in relation to the progression and prognosis of chronic kidney disease: A systematic review and dose-response meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0076.

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