title: Effect of hypoxia/reoxygenation on cell viability and expression and secretion of neurotrophic factors (NTFs) in primary cultured schwann cells.
abstract: As the primary myelin-forming cells of the peripheral nervous system, Schwann cells (SCs) play a key role in the regeneration of injured peripheral nerves. However, hypoxia causes injury of SCs, as observed in peripheral neuropathies, including those caused by diabetes. So we investigated the effect of hypoxia/reoxygenation (H/R) on SCs in this study. To do so, SCs were cultured in hypoxic condition in vitro and then in normal condition for 24 hr; The effects H/R on SCs were evaluated by MTT (3(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide) assay, Hoechst staining, immunocytochemistry, western blotting, ELISA, and RT-PCR. H/R resulted in a significant decrease in SCs survival and an increase in caspase-3 activity. H/R also reduced the mRNA level of BDNF (brain derived neurotrophic factor) and its secretion, but NGF mRNA level was elevated in these cells. These observations showed that H/R induces death of primary cultured SCs, and different mechanisms responsible for regulating NGF and BDNF expression.
authors.affiliation: Department of Anatomy, Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University Institutes of Medical Sciences, Shanghai, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Zhu
authors.forename: Feng
authors.initials: F
authors.lastname: Li
authors.forename: Wen-Juan
authors.initials: WJ
authors.lastname: Yu
authors.forename: Wen-Jin
authors.initials: WJ
authors.lastname: Wang
authors.forename: Liu
authors.initials: L
authors.lastname: Li
authors.forename: Li-Dan
authors.initials: LD
authors.lastname: Wan
authors.forename: Yan
authors.initials: Y
authors.lastname: Le
authors.forename: Wen-Long
authors.initials: WL
authors.lastname: Ding
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000502:physiology; D002478:Cells, Cultured; D003929:Diabetic Neuropathies / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015536:Down-Regulation / Q000502:physiology; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007511:Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009186:Myelin Sheath / Q000502:physiology / Q000648:ultrastructure; D020932:Nerve Growth Factor / Q000235:genetics / Q000378:metabolism; D009414:Nerve Growth Factors / Q000235:genetics / Q000378:metabolism*; D009416:Nerve Regeneration / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism*; D010523:Peripheral Nervous System Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012583:Schwann Cells / Q000378:metabolism*; D015854:Up-Regulation / Q000502:physiology; D014855:Wallerian Degeneration / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D009414:Nerve Growth Factors; D012333:RNA, Messenger; D020932:Nerve Growth Factor; D053148:Caspase 3; D010100:Oxygen