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Programmed cell death 5 suppresses AKT-mediated cytoprotection of endothelium

Seung-Hyun Lee1, Jaesung Seo1, Soo-Yeon Park1

  • 1Department of Biochemistry and Molecular Biology, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 03722 Seoul, Korea.

Proceedings of the National Academy of Sciences of the United States of America
|March 29, 2018
PubMed

Insights

Programmed cell death 5 (PDCD5) regulates endothelial function by modulating AKT-eNOS signaling, impacting vascular remodeling and nitric oxide production. Lower PDCD5 levels are linked to endothelial dysfunction and atherosclerosis risk factors.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Endothelial Cell Function

Background:

  • Programmed cell death 5 (PDCD5) is known for its role in cancer cell death.
  • Its specific function within the endothelium and its connection to atherosclerosis remain largely unexplored.

Purpose of the Study:

  • To investigate the role of PDCD5 in endothelial protein kinase B (PKB/AKT)-endothelial nitric oxide synthase (eNOS) signaling.
  • To determine if PDCD5 influences atherosclerosis development.

Main Methods:

  • Utilized endothelial-specific PDCD5 knockout mice and partial carotid ligation to study vascular remodeling.
  • Employed human umbilical vein endothelial cells (HUVECs) for knockdown experiments.
  • Analyzed interactions between PDCD5, histone deacetylase 3 (HDAC3), and AKT.
  • Measured AKT and eNOS phosphorylation and nitric oxide (NO) production.
  • Correlated serum PDCD5 levels with cardiovascular risk factors in a human cohort.

Main Results:

  • Endothelial PDCD5 knockout mice exhibited reduced vascular remodeling compared to wild-type mice.
  • PDCD5 competitively inhibited the interaction between HDAC3 and AKT.
  • PDCD5 knockdown in HUVECs accelerated HDAC3-AKT interaction, increased AKT and eNOS phosphorylation, and enhanced NO production.
  • Serum PDCD5 levels correlated with endothelial NO production, diabetes mellitus, HDL cholesterol, and coronary calcium.

Conclusions:

  • PDCD5 plays a crucial role in regulating endothelial function via the AKT-eNOS pathway.
  • PDCD5 is associated with endothelial dysfunction and may serve as a potential therapeutic target for atherosclerosis.
Keywords:
AKTHDAC3PDCD5atherosclerosisendothelium

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