Mammalian protein found in Homo sapiens
VGF or VGF nerve growth factor inducible is a secreted protein and neuropeptide precursor that may play a role in regulating energy homeostasis, metabolism[5] and synaptic plasticity.[6] The protein was first discovered in 1985 by Levi et al.[7] 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,[8][9][10][11][12][13][14][15] and TLQP-62 as well as AQEE-30 in regulating depression-like behaviors[16][17][18][19][20] and memory.[21][22] 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.[23] VGF expression is induced by NGF, CREB and BDNF and regulated by neurotrophin-3.[24] Physical exercise significantly increases VGF expression in mice hippocampal tissue and upregulates a neurotrophic signaling cascade thought to underlie the action of antidepressants.[16][25][26][27]
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[28] 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[29] and the expression of a fragment containing aminoacids 378-398 was found to be changing in amyotrophic lateral sclerosis[30] and Alzheimer's disease.[31] VGF expression has also been shown in damaged peripheral nerves, and it is thought to have a role in neuropathic pain.[32] 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.[33]
