Activation of PI3K/Akt prevents hypoxia/reoxygenation-induced GnRH decline via FOXO3a

Title:

Activation of PI3K/Akt prevents hypoxia/reoxygenation-induced GnRH decline via FOXO3a

Creator:

Guo, Han, Xuanyuan, Shuchuan, Zhang, Bensi, and Shi, Chun

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0bd2444f-03f5-42a5-ab0c-455b4db2a86e
uuid:0bd2444f-03f5-42a5-ab0c-455b4db2a86e
doi:10.33549/physiolres.934861

Subject:

hypoxia-reoxygenation, nuclear factor-κB, gonadotropinreleasing hormone, and forkhead box protein O3a

Type:

model:article and TEXT

Format:

počítač and online zdroj

Description:

Recent studies have suggested that the hypothalamus has an important role in aging by regulating nuclear factor-κB (NF-κB)-directed gonadotropin-releasing hormone (GnRH) decline. Moreover, our previous study has shown that ischemia-reperfusion (IR) injury activates NF-κB to reduce hypothalamic GnRH release, thus suggesting that IR injury may facilitate hypothalamic programming of system aging. In this study, we further examined the role of phosphoinositide 3-kinase (PI3K)/Protein kinase B (Akt) pathway, a critical intracellular signal pathway involved in the repair process after IR, in hypoxia-reoxygenation (HR)-associated GnRH decline in vitro. We used GT1-7 cells and primarily-cultured mouse GnRH neurons as cell models for investigation. Our data revealed that the activation of the PI3K/Akt/Forkhead box protein O3a (FOXO3a) pathway protects GnRH neurons from HR-induced GnRH decline by preventing HR-induced gnrh1 gene inhibition and NF-κB activation. Our results further the understanding of the regulatory mechanisms of HR-associated hypothalamic GnRH decline.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Coverage:

509-516

Source:

Physiological research | 2022 Volume:71 | Number:4

Harvested from:

CDK

Metadata only:

false