RESUMO
<p><b>OBJECTIVE</b>To investigate the effects and mechanisms of high glucose on the phenotype transformation of rat vascular smooth muscle cells (VSMCs).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>(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.</p><p><b>CONCLUSION</b>High glucose may promote phenotype transformation of VSMCs via the signal pathway of P38/MAPK.</p>
Assuntos
Animais , Ratos , Actinas , Metabolismo , Aorta Torácica , Biologia Celular , Western Blotting , Células Cultivadas , Glucose , Farmacologia , Imidazóis , Farmacologia , Sistema de Sinalização das MAP Quinases , Metaloproteinase 2 da Matriz , Metaloproteinase 9 da Matriz , Metabolismo , Músculo Liso Vascular , Biologia Celular , Miócitos de Músculo Liso , Biologia Celular , Osteopontina , Metabolismo , Fenótipo , Piridinas , Farmacologia , Proteínas Quinases p38 Ativadas por Mitógeno , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To investigate the effects of endothelia progenitor cells conditioned medium (EPC-CM) on the migration, adhesion and proliferation of vascular smooth muscle cells (VSMCs).</p><p><b>METHODS</b>Mononuclear cells were isolated from rat bone marrow by density gradient centrifugation,plated on dishes precoated with 5% fibronectin, and then cultured with complete M199 medium (including 15% fetal calf serum, 10 microg/L VEGF and 5 microg/L bFGF). EPC-CM was collected and used to incubate VSMCs isolated from rat arteriae aorta. After 24 h, VSMCs proliferation, adhesion and migration were assayed with CCK-8, adhesion test and modified Boyden chamber assay, respectively.</p><p><b>RESULTS</b>The proliferation, adhesion and migration of VSMCs were obviously decreased when the cells were cultured with EPC-CM.</p><p><b>CONCLUSION</b>EPC-CM could inhibit VSMC functions, which would be one of the mechanisms against atherosclerosis by EPCs.</p>