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Zhu X.-F.,Sun Yat Sen University | Shan Z.,Sun Yat Sen University | Ma J.-Y.,Sun Yat Sen University | Wang M.,Sun Yat Sen University | And 12 more authors.
Cellular Physiology and Biochemistry | Year: 2015

Aims: To explore the expression of MIR-24-3p in human arteries with arteriosclerosis obliterans (ASO) as well as the role of MIR-24-3p in the pathogenesis of ASO. Methods: We used quantitative real-time PCR (qRT-PCR) and in situ hybridization to monitor MIR-24-3p expression in human arteries. To investigate the effect of MIR-24-3p on human arterial smooth muscle cells (HASMCs), we applied cell counting and EdU assays to monitor proliferation and transwell and wound healing assays to investigate migration and flow cytometry to investigate apoptosis. Furthermore, we applied 3'-untranslated region (3'-UTR) luciferase assays to investigate the role of MIR-24-3p in targeting platelet-derived growth factor receptor B (PDGFRB) and c-Myc. Results: MIR-24-3p was mainly located in the media of arteries and was downregulated in ASO arteries compared with normal arteries. Platelet-derived growth factor BB (PDGF-BB) treatment reduced the expression of MIR-24-3p in primary cultured HASMCs. MIR-24-3p mimic oligos inhibited the proliferation and migration, and promotes apoptosis of HASMCs. Our 3'-UTR luciferase assays confirmed that PDGFRB and c-Myc were targets of MIR-24-3p. Conclusion: The results suggest that MIR-24-3p regulates the proliferation and migration of HASMCs by targeting PDGFRB and c-Myc. The PDGF/MIR-24-3p/PDGFRB and PDGF/MIR-24-3p/c-Myc pathways may play critical roles in the pathogenesis of ASO. These findings highlight the potential for new therapeutic targets for ASO. © 2015 S. Karger AG, Basel. Source

Yang C.-Q.,Sun Yat Sen University | Li W.,Sun Yat Sen University | Li W.,Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease | Li S.-Q.,Sun Yat Sen University | And 8 more authors.
Cellular Physiology and Biochemistry | Year: 2014

Objective: We investigated the molecular mechanism underlying the role of monocyte chemoattractant protein-1 (MCP-1) in the formation and development of human abdominal aortic aneurysm (AAA). Methods: We examined protein expression profiles using a protein array and found that MCP-1 was the most highly expressed protein in AAA tissues compared with normal aortas. To investigate the potential mechanism of MCP-1 involvement in the pathogenesis of AAA, we treated human aortic smooth muscle cells (HASMCs) with human recombinant MCP-1. Results: MCP-1 was the most highly expressed protein in AAA tissues compared with normal aorta; matrix metalloproteinase-9 (MMP-9) expression was also significantly increased. Treatment with MCP-1 significantly increased the expression and activation of MMP-9 and activated the three major mitogen activated protein kinases (MAPKs) extracellular signal regulated kinase (ERK), c-Jun amino terminal kinase (JNK1/2) and p38 MAPK. Furthermore, MCP-1-induced secretion of MMP-9 was inhibited by U0126 (inhibitor of the ERK 1/2 pathway) and SB203580 (inhibitor of the p38 MAPK pathway), but not SP600125 (inhibitor of the JNK1/2 pathway). Conclusion: These data demonstrate that MCP-1 stimulates secretion of MMP-9 directly through the ERK1/2 and p38 MAPK mediated pathways in HASMCs. Thus, inhibition of this molecular mechanism might be a potential therapeutic target in the non-surgical treatment of AAA. © 2014 S. Karger AG, Basel. Source

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