Non-receptor tyrosine kinase Src is required for ischemia-stimulated neuronal cell proliferation via Raf/ERK/CREB activation in the dentate gyrus.

BMC Neuroscience
He-Ping TianLi-Xin Li

Abstract

Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. However, Molecular mechanisms that regulate neuronal cell proliferation in the dentate gyrus (DG) following ischemic stroke insult are poorly understood. This study was designed to investigate the potential regulatory capacity of non-receptor tyrosine kinase Src on ischemia-stimulated cell proliferation in the adult DG and its underlying mechanism. Src kinase activated continuously in the DG 24 h and 72 h after transient global ischemia, while SU6656, the Src kinase inhibitor significantly decreased the number of bromodeoxyuridine (BrdU) labeling-positive cells of rats 7 days after cerebral ischemia in the DG, as well as down-regulated Raf phosphorylation at Tyr(340/341) site, and its down-stream signaling molecules ERK and CREB expression followed by 24 h and 72 h of reperfusion, suggesting a role of Src kinase as an enhancer on neuronal cell proliferation in the DG via modifying the Raf/ERK/CREB cascade. This hypothesis is supported by further findings that U0126, the ERK inhibitor, induced a reduction of adult hippocampal progenitor cells in DG after cerebral ischemia and down-regulated phospho-ERK and phospho-CREB expression,...Continue Reading

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Citations

Aug 7, 2012·Acta Pharmacologica Sinica·Nicholas L WeilingerRoger J Thompson
Mar 8, 2012·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Sudhirkumar U YanpallewarLino Tessarollo
Nov 3, 2010·Cellular and Molecular Life Sciences : CMLS·Koji Ohira
May 23, 2020·International Journal of Molecular Sciences·Yoo-Duk ChoiMihwa Kim

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