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Updated: Aug 27, 2025

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Long Noncoding RNA TPRG1-AS1 Suppresses Migration of Vascular Smooth Muscle Cells and Attenuates Atherogenesis via

Xiaoxiao Ren1, Huijuan Zhu1, Keyong Deng1

  • 1Key Laboratory of Cardiovascular Epidemiology and Department of Epidemiology, State Key Laboratory of Cardiovascular Disease (X.R., H.Z., K.D., X.N., D.L., B.Y., S.C., D.G., L.W.), Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Arteriosclerosis, Thrombosis, and Vascular Biology
|September 29, 2022
PubMed
Abstract

Insights

Long noncoding RNA TPRG1-AS1 inhibits human aortic smooth muscle cell migration by interacting with MYH9 protein. This interaction suppresses neointima formation and atherosclerosis, offering a potential therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Human aortic smooth muscle cell (HASMC) migration is a key factor in atherosclerosis development.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cardiovascular diseases.
  • The specific function of TPRG1-AS1 in HASMCs and atherosclerosis remains to be fully elucidated.

Purpose of the Study:

  • To functionally characterize the lncRNA TPRG1-AS1 in HASMCs.
  • To investigate the underlying mechanism of TPRG1-AS1 in HASMC migration, neointima formation, and atherosclerosis.
  • To determine the therapeutic potential of TPRG1-AS1 in cardiovascular pathology.

Main Methods:

  • Expression analysis of TPRG1-AS1 in atherosclerotic plaques using in silico and qRT-PCR.
  • Determination of TPRG1-AS1 full length, protein-coding capacity, and subcellular localization.
  • In vitro and in vivo functional studies, including loss- and gain-of-function experiments and animal models of vascular injury and atherosclerosis.

Main Results:

  • TPRG1-AS1 expression is significantly elevated in atherosclerotic plaques.
  • TPRG1-AS1 is a bona fide lncRNA (1279nt) localized in the cytoplasm and perinuclear regions of HASMCs.
  • TPRG1-AS1 directly interacts with MYH9 protein, promoting its degradation, inhibiting F-actin stress fiber formation, and consequently suppressing HASMC migration.
  • Overexpression of TPRG1-AS1 reduced neointima formation and attenuated atherosclerosis in Apoe-/- mice.

Conclusions:

  • TPRG1-AS1 acts as a suppressor of HASMC migration by interacting with MYH9 protein.
  • TPRG1-AS1 effectively inhibits neointima formation and atherosclerosis.
  • TPRG1-AS1 represents a potential therapeutic target for atherosclerosis.
Keywords:
RNA, long noncodingatherosclerosiscell movementmice, transgenic

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