Conclusions
TPM2 had an advantageous impact on ox-LDL-induced AS progression in vitro by mediating the RhoA pathway. This evidence might contribute to the therapy of AS.
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 (HAECs and VSMCs). An overexpression assay was performed to evaluate the role of TPM2 in AS. Meanwhile, the involvement of the RhoA pathway in TPM2-mediated AS progression was evaluated using narciclasine.
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 (HAECs and VSMCs). An overexpression assay was performed to evaluate the role of TPM2 in AS. Meanwhile, the involvement of the RhoA pathway in TPM2-mediated AS progression was evaluated using narciclasine.
Results
Tropomyosin 2 was dramatically upregulated in both AS tissues and ox-LDL-induced HAECs. Overexpression of TPM2 attenuated ox-LDL-stimulated cell growth depression, inflammatory and adhesive responses in HAECs, as well as oxidative stress and mitochondrial dysfunction. Additionally, VSMCs, impacted by TPM2-overexpressed HAECs, showed alleviated cellular processes which were abnormally activated by ox-LDL. Furthermore, depressed activation of the RhoA pathway was found in TPM2-overexpressed HAECs and activating the signaling rescued these effects of TPM2 exerted on ox-LDL-stimulated HAECs and VSMCs. Conclusions: TPM2 had an advantageous impact on ox-LDL-induced AS progression in vitro by mediating the RhoA pathway. This evidence might contribute to the therapy of AS.