Hibiscus sabdariffa polyphenols prevent palmitate-induced renal epithelial mesenchymal transition by alleviating dipeptidyl peptidase-4-mediated insulin resistance

2016 ◽  
Vol 7 (1) ◽  
pp. 475-482 ◽  
Author(s):  
Chien-Ning Huang ◽  
Chau-Jong Wang ◽  
Yi-Sun Yang ◽  
Chih-Li Lin ◽  
Chiung-Huei Peng
Keyword(s):  
Insulin Resistance ◽  
Diabetic Nephropathy ◽  
Epithelial Mesenchymal Transition ◽  
Dipeptidyl Peptidase ◽  
Socioeconomic Impact ◽  
Hibiscus Sabdariffa ◽  
Mesenchymal Transition ◽  
Dipeptidyl Peptidase 4

Diabetic nephropathy has a significant socioeconomic impact, but its mechanism is unclear and needs to be examined.

Polyphenols of Hibiscus sabdariffa Improved Diabetic Nephropathy via Attenuating Renal Epithelial Mesenchymal Transition

2013 ◽  
Vol 61 (31) ◽  
pp. 7545-7551 ◽  
Author(s):  
Yi-Sun Yang ◽  
Chau-Jong Wang ◽  
Chien-Ning Huang ◽  
Mu-Lin Chen ◽  
Ming-Jinn Chen ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Epithelial Mesenchymal Transition ◽  
Hibiscus Sabdariffa ◽  
Mesenchymal Transition

scholarly journals Dipeptidyl peptidase 4 promotes peritoneal fibrosis and its inhibitions prevent failure of peritoneal dialysis

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yi-Chen Li ◽  
Pei-Hsun Sung ◽  
Yao-Hsu Yang ◽  
John Y. Chiang ◽  
Hon-Kan Yip ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Epithelial Mesenchymal Transition ◽  
Dipeptidyl Peptidase ◽  
Diabetic Patients ◽  
Peritoneal Fibrosis ◽  
High Concentration ◽  
Mesenchymal Transition ◽  
Dipeptidyl Peptidase 4 ◽  
Stage Renal Disease ◽  
End Stage

AbstractPeritoneal dialysis (PD) possesses multiple advantages for end stage renal disease. However, long-term PD triggers peritoneal fibrosis (PF). From the nationwide analysis of diabetic PD patients (n = 19,828), we identified the incidence of PD failure was significantly lower in diabetic patients treated with dipeptidyl peptidase 4 (DPP4) inhibitors. Experimental study further showed high concentration of glucose remarkably enhanced DPP4 to promote epithelial-mesenchymal transition (EMT) in the mesothelial cells. In chlorhexidine gluconate (CG)-induced PF model of rats, DPP4 expression was enriched at thickening peritoneum. Moreover, as to CG-induced PF model, DPP4 deficiency (F344/DuCrlCrlj strain), sitagliptin and exendin-4 treatments significantly inhibited DPP4 to reverse the EMT process, angiogenesis, oxidative stress, and inflammation, resulting in the protection from PF, preservation of peritoneum and the corresponding functional integrity. Furthermore, DPP4 activity was significantly correlated with peritoneal dysfunction. Taken together, DPP4 caused peritoneal dysfunction/PF, whereas inhibition of DPP4 protected the PD patients against PD failure.

scholarly journals hsa-miR-199b-3p Prevents the Epithelial-Mesenchymal Transition and Dysfunction of the Renal Tubule by Regulating E-cadherin through Targeting KDM6A in Diabetic Nephropathy

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Shoujun Bai ◽  
Xiaoyan Xiong ◽  
Bo Tang ◽  
Tingting Ji ◽  
Xiaoying Li ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Renal Tubule ◽  
Epithelial Mesenchymal Transition ◽  
Kidney Tissue ◽  
Target Prediction ◽  
Luciferase Assay ◽  
Renal Tubules ◽  
Mesenchymal Transition ◽  
Hk2 Cells ◽  
E Cadherin

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. The association between epithelial-mesenchymal transition (EMT) and fibrosis is quite ascertained, but its link to eventual tubule dysfunction is missing. Here, we show that human microRNA- (hsa-miR-) 199b-3p protects renal tubules from diabetic-induced injury by repressing KDM6A, a histone lysine demethylase regulating E-cadherin expression. Lower E-cadherin expression is related to a higher level of KDM6A, while E-cadherin is promoted upon treatment with the KDM6A inhibitor GSK-J4 in both high glucose- (HG-) induced HK2 cells and the kidneys from streptozotocin- (STZ-) induced type 1 diabetic mice. However, overexpression or RNA silencing of E-cadherin fails to alter KDM6A expression. We also show that the upregulation of KDM6A is associated with the increased methylation level of the E-cadherin promoter. Then, the target prediction results and a dual-luciferase assay show that hsa-miR-199b-3p is a new miRNA that targets KDM6A. Overexpression of hsa-miR-199b-3p increases E-cadherin expression and prevents EMT through repressing KDM6A expression in HG-induced HK2 cells. In contrast, inhibitor-induced hsa-miR-199b-3p knockdown has opposite effects, as it decreases E-cadherin level and worsens EMT, accompanied by increased levels of KDM6A. Besides, Mir199b-knockout mice without mmu-miR-119b-3p expression exhibit more renal tubule dysfunction and more serious kidney tissue damage upon treatment with STZ. These results demonstrate that hsa-miR-199b-3p improves E-cadherin expression and prevents the progression of DN through targeting KDM6A. miR-199b-3p could be a future biomarker or target for the diagnosis or treatment of DN.

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