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Ox-LDL (oxidized low densitylipoprotein)-induced endothelial cell injury and dysfunction of vascular smooth muscle cell played critical roles in the development of atherosclerosis (AS). Tropomyosin 2 (TPM2) was indicated to be implicated in cardiac diseases, but its critical role and regulation mechanism in AS progression had not yet been elucidated.    Material and methods  The expression of TPM2 was investigated in AS tissues. Ox-LDL was used to construct an AS in vitro model based on endothelial and vascular smooth muscle cells (HAEC and VSMC). Overexpression assay was performed to evaluate the role of TPM2 in AS. Meanwhile, Narciclasine treatment analysed the involvement of RhoA pathway.    Results  TPM2 was dramatically upregulated both in AS tissues and ox-LDL-induced HAEC cells. The overexpression of TPM2 attenuated ox-LDL-stimulated cell growth depression, inflammatory and adhesive responses in HAEC, as well as oxidative stress and mitochondrial dysfunction. Besides, VSMC, impacted by TPM2-overexpressed HAEC, showed alleviated cellular processes which was abnormally activation induced by ox-LDL. Furthermore, the depressed activation of RhoA pathway was found in TPM2-overexpressed HAEC and activating the signaling rescued these effects of TPM2 exerted on ox-LDL-stimulated HAEC and VSMC.    Conclusions  TPM2 had an advantageous impact on ox-LDL-induced AS progression in vitro via mediating RhoA pathway. This evidence might be contributed to the therapy of AS.

Abnormal TPM2 expression is involved in the regulation of atherosclerosis progression via mediating RhoA signaling in vitro