TIM‑3 inhibits PDGF‑BB‑induced atherogenic responses in human artery vascular smooth muscle cells.

Mol Med Rep

Division of Vascular Surgery, Guangdong Key Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.

Published: August 2020

Increasing evidence suggests that T‑cell immunoglobulin and mucin domain 3 (TIM‑3) displays anti‑atherosclerotic effects, but its role in vascular smooth muscle cells (VSMCs) has not been reported. The present study aimed to investigate the function of TIM‑3 and its roles in human artery VSMCs (HASMCs). A protein array was used to investigate the TIM‑3 protein expression profile, which indicated that TIM‑3 expression was increased in the serum of patients with lower extremity arteriosclerosis obliterans disease (LEAOD) compared with healthy individuals. Immunohistochemistry and western blotting of arterial tissue further revealed that TIM‑3 expression was increased in LEAOD artery tissue compared with normal artery tissue. Additionally, platelet‑derived growth factor‑BB (PDGF‑BB) displayed a positive correlation with TIM‑3 expression in HASMCs. TIM‑3 decreased the migration and proliferation of PDGF‑BB‑induced HASMCs, and anti‑TIM‑3 blocked the effects of TIM‑3. The effect of TIM‑3 on the proliferation and migration of HASMCs was further investigated using LV‑TIM‑3‑transduced cells. The results revealed that TIM‑3 also inhibited PDGF‑BB‑induced expression of the inflammatory factors interleukin‑6 and tumor necrosis factor‑α by suppressing NF‑κB activation. In summary, the present study revealed that TIM‑3 displayed a regulatory role during the PDGF‑BB‑induced inflammatory reaction in HASMCs, which indicated that TIM‑3 may display anti‑atherosclerotic effects.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339574PMC
http://dx.doi.org/10.3892/mmr.2020.11167DOI Listing

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