| Cardiovascular complication is one of the main death reasons for patients with diabetes: to those suffering acute myocardial infarction (AMI),their mortality is 2 times that of general population; to those undergone percutaneous transluminal coronary angioplasty (PICA) the prevalence of restenosis is as high as 49%-71%, remarkably higher than those without diabetes. Restenosis poses severe threat to patients with coronary artery disease,especially with diabetic patients. Due to unknown mechanism of restenosis ,no effective treatment can be used ,so how to treat and prevent it remains a hot study over the world.Vascular remodeling is the common pathological character for both restenosis and diabetic angiopathy. Accumulation and altered composition of extracellular matrix (ECM) are the hallmark cause of vascular remodeling. It is no doubt that studying the mechanism of ECM formation and accumulation is an important step for preventing vascular remodeling. It has been proved that the formation and accumulation of ECM are under the modulation of transforming growth factor- P (TGF-P ). Related studies have indicated that TGF- & is an important growth factor. TGF- P is not only a potent regulator of the cells cycle in many types of cells, including vascular smooth muscle cells( VSMCs) and endothelial cells, but also a uniquely powerful fibrogenic cytokine. It has been shown that TGF- 3 induces the proliferation and migration of VSMCs and can promote ECM accumulation through different pathways, this growth factor has been postulated to play an important part in the occurence and development of vascular remodeling.After vascular injured, TGF-P is released from degranulated platelets and automatically produced by local cells. The increased expression of TGF-pmRNA was found in vascular walls with both patients and animal models of diabetic angiopathy and restenosis. Word et al demonstrated that the expression of mRNA of TGF-p,, TGF-p3 and TGF-p receptor(TGF-pR) II was significantly enhanced in vascular medium and endothelium by balloon injury . Smith et al also found that the expression level of TGF-p,, TGF~p2 and TGF-pRlImRNA showed an increase in endothelium of rat carotid artery balloon injury model compared with that in normal endothelium. The changes were correlated with the increase of mRNA expression of collagens type III and neoinrimal area, as well as reduction in lumen area. Yamanoto and Shankland observed that TGF-Pi mRNA expression began to increase 24h after the induction of diabetes. After 12-15 weeks of diabetes, a 2~3 fold increase occurred in diabetic rats than that in non-diabetic ones. TGF-pi mRNA in blood circulation was three times higher in diabetic rats than that in non-diabetic rats. The increase of glomerular TGF-P] mRNA expression in diabetic rats was suppressed by insulin treatment. A lot of evidence indicated a causal relationship between the increased production of TGF-P| and remodeling of ECM in diabetes. Bollineni and Ziyadeh et al reported that the high glucose-mediated synthesis of ECM proteins (collagen type I ,IV) in cultured mesangial cells was able to be reproduced by incubating mesangial cells with recombinant TCP-Pi in normal glucose. Addition of anti- TGF-P 1 antibodies reduced the effect of high glucose-stimulated collagen synthesis. Insulin treatment in streptozotocin-induced diabetic rats can reduce the diabetes-induced increase of both TGF-p , mRNA expression, and glomerular deposition of fibronectin and procollagen.Franzen et al confirmed that the different biological effects of TGF-p were mediated via specific membrane receptors, and by differential expression of TGF-PR. For example, TGF-PR I caused cell proliferation and TGF-PR II induced ECM accumulation. At present, there were a largenumber of studies upon the expression of TGF-pmRNA in kidney under the hyperglycaemia condition. But few studies were carried out on the expression of TGF-PR mRNA in renal, especially in macrovascular. Kanzak et al reported that the protein and mRNA expression of TGF-PR II and...
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