SRT1720-induced activation of SIRT1 alleviates vascular smooth muscle cell senescence through PKA-dependent phosphorylation of AMPKα at Ser485.,FEBS Open Bio

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SRT1720-induced activation of SIRT1 alleviates vascular smooth muscle cell senescence through PKA-dependent phosphorylation of AMPKα at Ser485.
FEBS Open Bio ( IF 2.8 ) Pub Date : 2020-06-05 , DOI: 10.1002/2211-5463.12895
Jin Young Sung _{1,

2} , Seul Gi Kim _{1,

2} , Du Hyong Cho _{1,

2} , Jae-Ryong Kim _{2,

3} , Hyoung Chul Choi _{1,

2}

Affiliation

Aging is a major risk factor for hypertension and atherosclerosis, and vascular smooth muscle cell (VSMC) senescence can promote aging‐related vascular diseases. Sirtuin‐1 (SIRT1) and AMP‐activated protein kinase (AMPK) were previously reported to modulate vascular senescence; however, its effects have not been well characterized. To determine the nature of the interaction between SIRT1 and AMPK in VSMC senescence, we investigated the effects of SRT1720 on its downstream targets of SIRT1 and the phosphorylation of AMPKα at Ser485. During Adriamycin‐induced VSMC senescence, SRT1720 increased the activity of SIRT1 and AMPKα phosphorylation at Ser485 via the cAMP–protein kinase A (PKA) pathway. Telomere length and telomerase reverse transcriptase expression were increased by SIRT1 activation with SRT1720. Taken together, these data show that activation of the SIRT1/cAMP–PKA/p‐AMPKα (Ser485) pathway may be an effective antisenescence mechanism for VSMCs.

中文翻译：

SRT1720 诱导的 SIRT1 激活通过 AMPKα 在 Ser485 的 PKA 依赖性磷酸化减轻血管平滑肌细胞衰老。

衰老是高血压和动脉粥样硬化的主要危险因素，血管平滑肌细胞（VSMC）衰老可促进衰老相关的血管疾病。Sirtuin-1 (SIRT1) 和 AMP 活化蛋白激酶 (AMPK) 先前被报道可调节血管衰老；然而，其影响尚未得到很好的表征。为了确定 SIRT1 和 AMPK 在 VSMC 衰老中相互作用的性质，我们研究了 SRT1720 对其下游靶标 SIRT1 的影响以及 AMPKα 在 Ser485 处的磷酸化。在阿霉素诱导的 VSMC 衰老过程中，SRT1720 通过 cAMP-蛋白激酶 A（PKA）途径增加了 SIRT1 的活性和 Ser485 处的 AMPKα 磷酸化。通过 SRT1720 激活 SIRT1，端粒长度和端粒酶逆转录酶表达增加。综合起来，

更新日期：2020-06-05

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