RGC-32' dual role in smooth muscle cells and atherogenesis.
Clin Immunol
; 238: 109020, 2022 05.
Article
en En
| MEDLINE
| ID: mdl-35462050
ABSTRACT
Proliferation of endothelial cells (EC) and smooth muscle cells (SMC) is a critical process in atherosclerosis. Here, we investigated the involvement of sublytic C5b-9 effector Response Gene to Complement 32 (RGC-32) in cell cycle activation, phenotypic switch, and production of extracellular matrix (ECM) in SMC. Overexpression of RGC-32 augmented C5b-9-induced cell cycle activation and proliferation of SMC in an ERK1-dependent manner and silencing of RGC-32 inhibited C5b-9-induced cell cycle activation. C5b-9-induced cell cycle activation also required phosphorylation of RGC-32 at threonine 91. We found that ECM components fibronectin and collagens I-V were expressed by SMC in human aortic atherosclerotic tissue. Silencing of RGC-32 in cultured SMC was followed by a significant reduction in TGF-ß-induced expression of SMC differentiation markers myocardin, SM22 and α-SMA, and that of collagens I, IV and V. These data suggest that RGC-32 participates in both sublytic C5b-9-induced cell cycle activation and TGF-ß-induced ECM production.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Complejo de Ataque a Membrana del Sistema Complemento
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Proteínas de Ciclo Celular
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Aterosclerosis
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Proteínas Musculares
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Proteínas del Tejido Nervioso
Límite:
Humans
Idioma:
En
Año:
2022
Tipo del documento:
Article