Tempol effect on epithelial-mesenchymal transition induced by hyperglycemia

Abstract

BackgroundOne of common mechanisms in pathophysiology of chronic kidney diseases is epithelial-mesenchymal transition (EMT). On the other hand oxidative stress has been known to participate in kidney damage of diabetic nephropathy (DN). ObjectivesWe studied if tempol, a well-known antioxidant agent, can ameliorate EMT in DN induced in male rats. Materials and MethodsTwenty-seven male rats were equally divided in to 4 groups. Group I (control or C), group II (diabetic or D), group III (T) rats which was given tempol (100 mg/kg/day) by gavages for 28 days and group IV (D&T) was diabetic rats that also received same dose of tempol. After treatment, their kidneys were studied by immunohistochemicalstaining. ResultsPathological changes in the kidney were detected concurrently with increasing kidney weight and urinary albumin excretion. In addition, EMT indices, i.e. decline of E-cadherin and increase of α SMA staining were significantly emerged in the renal tubular cells of diabetic group and were partially modified in diabetic group which were simultaneously treated by tempol. ConclusionsTempol can modify, but not significantly, EMT induced by DN.

Hyperglycemia activates the renin-angiotensin system and induces epithelial-mesenchymal transition in streptozotocin-induced diabetic kidneys

“…Hyperglycemia induces EMT in podocytes and renal tubular epithelial cells and leads to renal fibrosis in diabetic nephropathy. 13 The effect of hyperglycemia on intrarenal RAS component expression remains controversial. 11 , 12 In the experimental gerbil model of DM, we found that hyperglycemia resulted in distortion and disruption of kidney morphology, increased oxidative stress and inflammatory markers, and increased profibrotic growth factor and RAS component expression.…”

“… 12 Hyperglycemia induced EMT in podocytes and renal tubular epithelial cells and led to renal fibrosis and dysfunction in experimental animals with diabetic nephropathy and patients with DM. 13 However, the connection between the RAS and transforming growth factor (TGF)-β in EMT remains largely unknown. We hypothesized that hyperglycemia activates the RAS and induces EMT and renal fibrosis in an animal model of DM.…”

The various role of microRNAs in breast cancer angiogenesis, with a special focus on novel miRNA-based delivery strategies

“…Vascular permeability increases, and the vessel wall deteriorates locally (i.e., extracellular matrix (ECM) or basement membrane), marking the initial step's start. Endothelial cells join the stroma of the tumor, migrate against a signal like vascular endothelial growth factor (VEGF) or fibroblast growth factor (FGF), and they proliferate behind the cutting hand [17,18]. Since they lack defense from other cell types, the cells may be more vulnerable to agents that interfere with their proliferation at this time [19,20].…”

A Nucleoside/Nucleobase-Rich Extract from Cordyceps Sinensis Inhibits the Epithelial–Mesenchymal Transition and Protects against Renal Fibrosis in Diabetic Nephropathy

“…Myofibroblasts play the foremost role in the progression of renal fibrosis in DN, while the origin of the fibroblasts remains elusive. In addition to the activation of residential fibroblasts, EMT is considered to be a direct contributor to the kidney population of myofibroblasts [36,37]. The EMT formation in tubular epithelial cells plays a significant role in TIF, which is a hallmark of DN [38,39].…”