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Cdk5 is required for the neuroprotective effect of transforming growth factor-β1 against cerebral ischemia-reperfusion

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [2];  [3]; ; ;  [1];  [4]
  1. Department of Physiology and Neurobiology, Xinxiang Medical University (China)
  2. Department of Toxicology, School of Public Health, Xinxiang Medical University (China)
  3. College of Physical Education, Shanxi University (China)
  4. School of Life Science and Technology, Xinxiang Medical University (China)
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.
OSTI ID:
22696966
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 485; ISSN 0006-291X; ISSN BBRCA9
Country of Publication:
United States
Language:
English

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