[The effects and mechanisms of high glucose on the phenotype transformation of rat vascular smooth muscle cells].
Jing Zhang, Hairong Chu, Ying Guo, Jianhua Liu, Wenping Li, Hong Li, Min Cheng
Abstract
Jing Zhang, Hairong Chu, Ying Guo, Jianhua Liu, Wenping Li, Hong Li, Min Cheng
Abstract
OBJECTIVE: To investigate the effects and mechanisms of high glucose on the phenotype transformation of rat vascular smooth muscle cells (VSMCs). METHODS: VSMCs ere isolated from rat thoracic aorta and the 3rd-5th VSMCs were incubated with normal glucose (5.5 mmol/L), high glucose (25 mmol/L), or high glucose (25 mmol/L) + P38 inhibitor (25 mmol/L +SB203580) for another 24 hours. Then the gene expression of osteopontin (OPN), alpha smooth-actin (alpha-SMA), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9(MMP-9) were assayed by real time RT-PCR, the protein expression of P38 were assayed by Western blot. RESULTS: (1) High glucose promoted the phenotype transformation of VSMCs and up-regulated the expression of MMP-2 and MMP-9. (2) High glucose promoted the phosphorylation of P38. (3) SB203580, the inhibitor of P38/MAPK signal pathway, inhibited the effects of high glucose on phenotype transformation and expression of MMP-2 and MMP-9. CONCLUSION: High glucose may promote phenotype transformation of VSMCs via the signal pathway of P38/MAPK.
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OBJECTIVE: To investigate the effects and mechanisms of high glucose on the phenotype transformation of rat vascular smooth muscle cells (VSMCs). METHODS: VSMCs ere isolated from rat thoracic aorta and the 3rd-5th VSMCs were incubated with normal glucose (5.5 mmol/L), high glucose (25 mmol/L), or high glucose (25 mmol/L) + P38 inhibitor (25 mmol/L +SB203580) for another 24 hours. Then the gene expression of osteopontin (OPN), alpha smooth-actin (alpha-SMA), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9(MMP-9) were assayed by real time RT-PCR, the protein expression of P38 were assayed by Western blot. RESULTS: (1) High glucose promoted the phenotype transformation of VSMCs and up-regulated the expression of MMP-2 and MMP-9. (2) High glucose promoted the phosphorylation of P38. (3) SB203580, the inhibitor of P38/MAPK signal pathway, inhibited the effects of high glucose on phenotype transformation and expression of MMP-2 and MMP-9. CONCLUSION: High glucose may promote phenotype transformation of VSMCs via the signal pathway of P38/MAPK.
Key concepts: Vascular smooth muscle, Osteopontin, Matrix metalloproteinase, Phenotype, Western blot, p38 mitogen-activated protein kinases, Transformation (genetics), Biology