FGF9-induced changes in cellular redox status and HO-1 upregulation are FGFR-dependent and proceed through both ERK and AKT to induce CREB and Nrf2 activation
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- 作者：Jih-Ing Chuanga ; b ; jichuang@mail.ncku.edu.tw" class="auth_mail" title="E-mail the corresponding author ; Jui-Yen Huanga ; c ; Shaw-Jenq Tsaia ; b ; H. Sunny Suna ; d ; Shang-Hsun Yanga ; b ; Pei-Chin Chuange ; Bu-Miin Huanga ; f ; Cheng-Hsin Chingb
- 关键词：PD ; Parkinson disease ; γ-GCSc ; γ-glutamylcysteine synthetase catalytic subunit ; HO-1 ; heme oxygenase-1 ; FGF9 ; fibroblast growth factor 9 ; MPP+ ; 1-methyl-4-phenylpyridinium ; CREB ; cAMP-response element binding protein ; Nrf2 ; nuclear factor erythroid-derived 2-like 2 ; SN ; substantia nigra
- 刊名：Free Radical Biology and Medicine
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：89
- 期：Complete
- 页码：274-286
- 全文大小：3084 K
文摘
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FGF9-induced HO-1 and γ-GCS expression was prevented by an FGFR inhibitor, PD173014.
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FGF9 induced ERK and AKT phosphorylation and CREB and Nrf2 activation in neurons.
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ERK or AKT inhibition prevented FGF9 antioxidative functions and neuroprotection.
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Knockdown of CREB or Nrf2 blocked FGF9 functions, but not ERK and AKT activity.
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FGF9-induced HO-1 and γ-GCS upregulation is mediated by the FGFR/ERK, AKT/CREB and Nrf2 signaling pathway.