RIP2 Knockdown Attenuates Vascular Smooth Muscle Cells Activation via Negative Regulating Myocardin Expression

Abstract Background RIP2 is an adaptor protein contributing to the activation of nuclear factor-κB induced by TNF receptor-associated factor (TRAF) and nucleotide oligomerization domain (NOD)-dependent signaling implicated in innate and adaptive immune response. Beyond regulation of immunity, we aim...

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Published in:American journal of hypertension 2022-05, Vol.35 (5), p.454-461
Main Authors: Zhang, Lan, Huang, Qian-wei, Pu, Yan-fen, Xiao, Xiao-qiang, Song, Bian-jing, Zhang, Xue-ping, Yang, Yong-sheng, Zhang, Yu-song, Gong, Fu-han
Format: Article
Language:English
Subjects:
Becaplermin - metabolism
Becaplermin - pharmacology
Cell Movement
Cell Proliferation
Cells, Cultured
Humans
Hyperplasia - metabolism
Hyperplasia - pathology
Muscle, Smooth, Vascular - cytology
Myocytes, Smooth Muscle - metabolism
Nuclear Proteins - metabolism
Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics
Trans-Activators - metabolism
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Summary:Abstract Background RIP2 is an adaptor protein contributing to the activation of nuclear factor-κB induced by TNF receptor-associated factor (TRAF) and nucleotide oligomerization domain (NOD)-dependent signaling implicated in innate and adaptive immune response. Beyond regulation of immunity, we aimed to elucidate the role of RIP2 in vascular smooth muscle cell (VSMC) phenotypic modulation. Methods and results In the current study, we observed that RIP2 showed an increased expression in VSMCs with PDGF-BB stimulation in a dose-dependent manner. Knockdown of RIP2 expression mediated by adenovirus dramatically accelerated the expression of VSMC-specific differentiation genes induced by PDGF-BB. Silencing of RIP2 inhibited proliferative and migratory ability of VSMCs. Additionally, we demonstrated that RIP2 knockdown can promoted myocardin expression. Furthermore, RIP2 inhibition also can attenuate the formation of intimal hyperplasia. Conclusions These findings suggested that RIP2 played an important role in regulation of VSMCs differentiation, migration, and proliferation that may due to affect myocardin expression. Our results indicated that RIP2 may be a novel therapeutic target for intimal hyperplasia. Graphical Abstract Graphical Abstract RIP2 was upregulated in PDGF-BB-treated VSMCs. RIP2 knockdown significantly regulated VSMC phenotypic switching, with decreased proliferation, migration, and dedifferentiation. RIP2 silencing substantially increased myocardin expression.
ISSN:0895-7061
1941-7225
DOI:10.1093/ajh/hpac009