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Updated: Nov 19, 2025

Inducible and Reversible Dominant-negative DN Protein Inhibition
Published on: January 7, 2019
BOP1 Knockdown Attenuates Neointimal Hyperplasia by Activating p53 and Inhibiting Nascent Protein Synthesis
Fangyuan Jia1,2,3, Qi Wu1,2,3, Zhiwei Wang1,2,3
1Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, 238# Jiefang Road, Wuhan, 430000 Hubei Province, China.
Abstract:
The rate of ribosome biogenesis plays a vital role in cell cycle progression and proliferation and is strongly connected with coronary restenosis and atherosclerosis. Blocking of proliferation 1 (BOP1) has been found as an evolutionarily conserved gene and a pivotal regulator of ribosome biogenesis and cell proliferation. However, little is known about its role in neointimal formation and its relationship with vascular smooth muscle cell (VSMC) proliferation and migration. The present study mainly explores the effect of BOP1 on VSMCs, the progression of neointimal hyperplasia, and the pathogenic mechanism. The expression of BOP1 was found to be significantly elevated during neointimal formation in human coronary samples and the rat balloon injury model. BOP1 knockdown inspires the nucleolus stress, which subsequently activates the p53-dependent stress response pathway, and inhibits the nascent protein synthesis, which subsequently inhibits the proliferation and migration of VSMCs. Knockdown ribosomal protein L11 (RPL11) by transfecting with siRNA or inhibiting p53 by pifithrin-α (PFT-α) partly reserved the biological effects induced by BOP1 knockdown. The present study revealed that BOP1 deletion attenuates VSMC proliferation and migration by activating the p53-dependent nucleolus stress response pathway and inhibits the synthesis of nascent proteins. BOP1 may become a novel biological target for neointimal hyperplasia.
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