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Updated: Sep 25, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
LncRNA LINC00281/Annexin A2 Regulates Vascular Smooth Muscle Cell Phenotype Switching via the Nuclear Factor-Kappa B
Lan Cheng1, Huan Wang2, ReneNfornah Maboh1
1The Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Abstract:
Abnormal phenotype switch in vascular smooth muscle cells (VSMCs) plays an important role in the initiation and progression of vascular proliferative diseases. Annexin A2 (ANXA2), related to the pro-inflammatory response, contributes to the proliferation and migration of VSMCs. This study explored the mechanisms involved in the regulation of VSMC phenotype modulation via ANXA2. The results revealed that ANXA2 promotes the phosphorylation of p65 and co-translocates with p65 into the nucleus, resulting in VSMC proliferation, migration, and dedifferentiation. Based on bioinformatics predictions and RNA immunoprecipitation assays, LINC00281 was confirmed to be an upstream regulator of ANXA2. Taken together, ANXA2, which is negatively regulated by the long noncoding RNA (lncRNA) LINC00281, has significant importance in the regulation of VSMC proliferation, migration, and phenotype switching via the nuclear factor-kappa B (NF-кB) p65 signaling pathway. This indicates that the lncRNA LINC00281/ANXA2/NF-кB p65 signaling pathway might be a new therapeutic target for vascular proliferative diseases.
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