VGF
Template:Short description Template:Others Template:Infobox gene
VGF or VGF nerve growth factor inducible is a secreted protein and neuropeptide precursor that may play a role in regulating energy homeostasis, metabolism[1] and synaptic plasticity.[2] The protein was first discovered in 1985 by Levi et al.[3] in an experiment with PC12 cells and its name is non-acronymic. VGF gene encodes a precursor which is divided by proteolysis to polypeptides of different mass, which have a variety of functions, the best studied of which are the roles of TLQP-21 in the control of appetite and inflammation,[4][5][6][7][8][9][10][11] and TLQP-62 as well as AQEE-30 in regulating depression-like behaviors[12][13][14][15][16] and memory.[17][18] The expression of VGF and VGF-derived peptides is detected in a subset of neurons in the central and peripheral nervous systems and specific populations of endocrine cells in the adenohypophysis, adrenal medulla, gastrointestinal tract, and pancreas.[19] VGF expression is induced by NGF, CREB and BDNF and regulated by neurotrophin-3.[20] Physical exercise significantly increases VGF expression in mice hippocampal tissue and upregulates a neurotrophic signaling cascade thought to underlie the action of antidepressants.[12][21][22][23]
Role in pathology
Changes in expression of discrete VGF fragments have been detected in different neurological and psychiatric conditions. In schizophrenia, one study has shown an increase in the VGF23-62 peptide[24] and a subsequent small study demonstrated that drugs further increase the expression, pointing at a possible ameliorating action of the fragment. A decreased expression of VGF26-62 peptide was found in frontotemporal dementia[25] and the expression of a fragment containing aminoacids 378-398 was found to be changing in amyotrophic lateral sclerosis[26] and Alzheimer's disease.[27] VGF expression has also been shown in damaged peripheral nerves, and it is thought to have a role in neuropathic pain.[28] In glioblastoma, VGF has been shown to play autocrine and paracrine roles in feedback loops between differentiated glioblastoma cells and glioblastoma-specific cancer stem cells, promoting growth, survival and self-renewal.[29]
References
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