2. Academic Validation
  3. A novel role for YPEL2 in mediating endothelial cellular senescence via the p53/p21 pathway

A novel role for YPEL2 in mediating endothelial cellular senescence via the p53/p21 pathway

  • Mech Ageing Dev. 2023 Mar 22;111803. doi: 10.1016/j.mad.2023.111803.
Jian-Xiong Xu 1,  Mao-Lin Tang 2,  Zhi-Feng Lu 3,  Yu Song 2,  Ke-Lan Zhang 2,  Run-Chao He 2,  Xiang-Na Guo 1,  Yun-Qi Yuan 1,  Xiaoyan Dai 4,  Xin Ma 5
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
  • 2 Department of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
  • 3 Department of Clinical Laboratory, Affiliated Dongguan People's Hospital, Southern Medical University, Dongguan, China.
  • 4 Key Laboratory of Molecular Target & Clinical Pharmacology and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 511436, China. Electronic address: xdai@gzhmu.edu.cn.
  • 5 Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. Electronic address: maxinfly@126.com.
PMID: 36963468 DOI: 10.1016/j.mad.2023.111803
Abstract

Yippee-like 2 (YPEL2) is expressed in tissues and organs enriched in vascular networks, such as heart, kidney, and lung. However, the roles of YPEL2 in endothelial cell senescence and the expression of YPEL2 in atherosclerotic plaques have not yet been investigated. Here, we report the essential role of YPEL2 in promoting senescence in human umbilical vein endothelial cells (HUVECs) and the upregulation of YPEL2 in human atherosclerotic plaques. YPEL2 was significantly upregulated in both H2O2-induced senescent HUVECs and the arteries of aged mice. Endothelial YPEL2 deficiency significantly decreased H2O2-increased senescence-associated beta-galactosidase (SA-β-gal) activity and reversed H2O2-inhibited cell viability. Additionally, endothelial YPEL2 knockdown reduced H2O2-promoted THP-1 cell adhesion to HUVECs and downregulated ICAM1 and VCAM1 expression. Mechanistic studies divulged that the p53/p21 pathway was involved in YPEL2-induced cellular senescence. We conclude that YPEL2 promotes cellular senescence via the p53/p21 pathway and that YPEL2 expression is elevated in atherosclerosis. These findings reveal YPEL2 as a potential therapeutic target in aging-associated diseases.

Keywords

YPEL2; atherosclerosis; endothelial cell; p53; senescence.

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