Abstract
BackgroundAbnormal proliferation and migration of vascular smooth muscle cells (VSMCs) accelerated vascular diseases progression, like atherosclerosis and restenosis. MicroRNAs were reported to participate in modulating diverse cellular processes. Here, we focused on exploring the role of miR-638 in VSMCs glycolysis and underlying mechanism.MethodsCell Counting Kit-8 (CCK-8) assay was used to measure cell viability. Western blot assay was conducted to determine the expression of cell proliferation markers proliferating cell nuclear antigen (PCNA) and Ki-67, as well as Lactate dehydrogenase A (LDHA). VSMCs migration and invasion were evaluated by Transwell assay. Luciferase reporter gene assay and RNA immunoprecipitation were performed to validate the target relationship between miR-638 and LDHA. LDHA and miR-638 expression were also determined. Glycolysis of VSMCs was tested by corresponding Kits.ResultsPlatelet-derived growth factor-bb (PDGF-bb) promoted the VSMCs viability and down-regulated miR-638. Overexpression of miR-638 inhibited cell proliferation, migration and invasion of VSMCs. LDHA was identified as a target of miR-638, and counter-regulated by miR-638. Loss of miR-638 attenuated the suppressor effects on the proliferation, migration and invasion of VSMCs induced by LDHA down-regulation. MiR-638 inhibited the glycolysis of VSMCs by targeting LDHA.ConclusionMiR-638 is down-regulated by PDGF-bb treatment and suppressed the glycolysis of VSMCs via targeting LDHA.
Highlights
Cardiovascular diseases, such as coronary artery disease, atherosclerosis, heart attack, are a leading cause of mortality in the world [1]
MiR-638 is down-regulated by Platelet-derived growth factor-bb (PDGF-bb) treatment and suppressed the glycolysis of vascular smooth muscle cells (VSMCs) via targeting Lactate dehydrogenase A (LDHA)
The cell viability of VSMCs showed an obvious augment after treatment with 30 ng/mL PDGF-bb, compared with that in control group, and the cell viability increased in a time-dependent manner (Fig. 1A)
Summary
Cardiovascular diseases, such as coronary artery disease, atherosclerosis, heart attack, are a leading cause of mortality in the world [1]. The atherosclerosis, regulation and function of vascular smooth muscle cells (VSMCs) are crucial in its progression [2]. VSMCs were regarded as a necessary component of the vascular system to maintain vascular integrity [3], and the abnormal proliferation of VSMCs was suggested to be associated with the pathogenesis of cardiovascular diseases [4]. Several reports have proved that introduction of PDGF-bb effectively promote cell proliferation and migration of VSMCs [6, 7]. Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) accelerated vascular diseases progression, like atherosclerosis and restenosis. We focused on exploring the role of miR-638 in VSMCs glycolysis and underlying mechanism. Proliferation, migration and invasion of VSMCs induced by LDHA down-regulation. MiR-638 inhibited the glycolysis of VSMCs by targeting LDHA
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