17β-Estradiol Prevents the Glutamate-Induced Decrease of Akt and Its Downstream Targets in HT22 Cells

Journal of Veterinary Medical Science

Phil-Ok KOH¹ 

[1] Department of Anatomy, College of Veterinary Medicine and Institute of Agriculture and Life Science, Gyeongsang National University

关键词: Akt;    Bad;    estradiol;    FKHR;    FKHRL1;   

DOI  :  10.1292/jvms.69.285

学科分类：兽医学

来源: Japanese Society of Veterinary Science

【 摘 要 】

References(14)Cited-By(6)Estradiol is known to exert neuroprotective effect against glutamate toxicity in hippocampal-derived cell line (HT22). This study investigated whether estradiol modulates the anti-apoptotic signal through the phosphorylation of Akt and its downstream targets, including Bad, forkhead transcription factors FKHR and FKHRL1. Pretreatment with 17β-estradiol decreased glutamate toxicity-induced cell death in HT22 cells. Also, pretreatment with 17β-estradiol significantly decreased the positive cells of TUNEL stain, compared to that of only glutamate-treated cells. Potential activation was measured by phosphorylation of Akt at Ser473, Bad at Ser136, FKHR at Ser256, and FKHRL1 at Thr32 using Western blot analysis. 17β-estradiol pretreatment prevented the glutamate-induced decrease of pAkt, pBad, pFKHR, and pFKHRL1. These findings clearly confirm that 17β-estradiol plays a potent neuroprotective role against glutamate-induced toxicity and suggest that phosphorylation of Akt and its downstream targets by 17β-estradiol mediated these protective effects.

【 授权许可】

Unknown