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Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
Cdk5 is required for the neuroprotective effect of transforming growth factor-β1 against cerebral
Wenhui Zhao1, Jing Yan1, Liyun Gao2
1Department of Physiology and Neurobiology, Xinxiang Medical University, China; Sino-UK Joint Laboratory of Brain Functions and Injury, Science and Technology Department of Henan Province, China.
Abstract:
Transforming Growth Factor β1 (TGF-β1), a well-known neuroprotective and neurotrophic factor in the central nervous system, is also involved in the repair process responses after ischemia-reperfusion injury. Herein, we found that TGF-β1 enhanced Cdk5 expression while decreased Tunel-positive cells compared with the ischemia group, and roscovitine(Cdk5 inhibitor) treatment could blunt these effects. In vitro study, TGF-β1 facilitated Cdk5/p35 complex, the proliferation, neurite growth and differentiation of PC12 cells, effects of which could be blunted by roscovitine and Cdk5 silencing. Moreover, ERK1/2 inhibitor SCH772984 abrogated the effects of TGF- β1 on Cdk5 and Bax levels. Taken together, we conclude that Cdk5 contributes to the neuroprotective function of TGF- β1 via ERK1/2 signaling.
