Effects of Nogo-A receptor antagonist on the regulation of the Wnt signaling pathway and neural cell proliferation in newborn rats with hypoxic ischemic encephalopathy.

Abstract	Hypoxic ischemic encephalopathy is a serious condition due to inadequate oxygen supply to the brain. Regeneration of neural cells is a critical process for repairing the damaged brain. Nogo has been identified as an inhibitor of neurite outgrowth that is specific to the brain. In the present study, the Nogo-A receptor (NgR) antagonist NEP1-40 was used to study the effects of inhibition of NgR on the regeneration of neural cells and the related Wnt signaling pathway in newborn rats. The investigation focused on the transcription factors regulated in the Wnt signaling pathway during the repair process, together with the proliferation of neural cells. The results indicated that c-Jun and c-Myc were the main transcription factors involved in the Wnt signaling pathway, while neural cell proliferation in the subventricular zone was increased during this process.
Authors	Yongxiang Wang, Jiaxiang Gu, Xinmin Feng, Hua Wang, Yuping Tao, Jingcheng Wang
Journal	Molecular medicine reports (Mol Med Rep) Vol. 8 Issue 3 Pg. 883-6 (Sep 2013) ISSN: 1791-3004 [Electronic] Greece
PMID	23842701 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Ki-67 Antigen Myelin Proteins NEPI-40 protein, rat Nogo Proteins Peptide Fragments Proto-Oncogene Proteins c-myc Rtn4 protein, rat 8-epi-prostaglandin F2alpha Dinoprost JNK Mitogen-Activated Protein Kinases
Topics	Animals Animals, Newborn Cell Proliferation (drug effects) Dinoprost (analogs & derivatives, analysis) Disease Models, Animal Enzyme-Linked Immunosorbent Assay Hypoxia-Ischemia, Brain (drug therapy, metabolism, pathology) JNK Mitogen-Activated Protein Kinases (metabolism) Ki-67 Antigen (metabolism) Male Myelin Proteins (antagonists & inhibitors, metabolism, pharmacology, therapeutic use) Nerve Regeneration (drug effects) Neurons (cytology, metabolism) Nogo Proteins Peptide Fragments (pharmacology, therapeutic use) Proto-Oncogene Proteins c-myc (metabolism) Rats Rats, Wistar Up-Regulation (drug effects) Wnt Signaling Pathway (drug effects)

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