Effect of LINC00707 on proliferation, migration and inflammatory factors of human vascular smooth muscle cells induced by ox-LDL by targeting miR-30c-5p / 中国药理学通报

ABSTRACT

Aim To explore the effect of LINC00707 on the proliferation, migration and inflammatory factors of human vascular smooth muscle cells induced by oixidized low-density lipoprotein (ox-LDL) and its possible mechanism. Methods ox-LDL was used to induce human vascular smooth muscle cells (HVSMCs) to establish an atherosclerotic cell model. si-NC, siLINC00707, miR-NC, miR-30c-5p mimic were trans-fected into HVSMCs, and then 100 mg • L~ ox-LDL was added to the cells. si-LINC00707 and anti-miRNC, or si-LINC00707 and miR-30c-5p Inhibitor were co-transfected into HVSMCs and then treated with 100 mg • L ox-LDL. qRT-PCR was used to detect the expression of LINC00707 and miR-30c-5p. CCK-8 and Transwell test were used to detect cell proliferation and migration. ELISA was used to detect the levels of IL-6, TNF-a, and IL-10. The dual-luciferase reporter experiment was used to detect the targeting relationship between LINC00707 and miR-30c-5p. Western blot was used to detect the protein expression of E-cadherin and N-cadherin. Results The expression of LINC00707 in HVSMCs induced by ox-LDL increased (P <0. 05), while the expression of miR-30c-5p decreased (P < 0. 05). After transfection with siLINC00707 or miR-30c-5p mimic, cell viability, the protein level of N-cadherin, the levels of IL-6 and TNF-a decreased (P < 0. 05), and the number of im grating cells decreased (P<0. 05), while the protein level of E-coadherin and the level of IL-10 increased (P <0. 05). LINC00707 could target miR-30c-5p. After co-transfection with si-LINC00707 and miR-30c-5p inhibitor, cell survival rate, the protein level of N-cadherin, the levels of IL-6 and TNF-α increased (P < 0.05), and the number of migrating cells increased (P <0. 05), while the protein level of E-cadherin and the level of IL-10 decreased (P < 0. 05). Conclusion Down-regulation of the expression of LINC00707 could inhibit the proliferation, migration and inflammation of human vascular smooth muscle cells induced by ox-LDL by promoting the expression of miR-30c-5p.