1,25(OH)2D3/VDR attenuates high glucose-induced epithelial-mesenchymal transition in human peritoneal mesothelial cells via the TGFβ/Smad3 pathway

Yang, Lina; Wu, Lan; Zhang, Xiuli; Hu, Ye; Fan, Yi; Ma, Jun

doi:10.3892/mmr.2017.6276

Cited by 21 publications

(15 citation statements)

References 29 publications

(25 reference statements)

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“…Vitamin D analogs can suppress matrix-producing myofibroblast activation by upregulating the expression of anti-fibrotic hepatocyte growth factor in renal interstitial fibroblasts [ 123 ]. In human peritoneal mesothelial cells, inhibitory effects of VDR agonists on EMT have also been reported [ 124 , 125 ].…”

Section: Renoprotective Mechanisms Of Vdrmentioning

confidence: 99%

Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases

Yang

Wang

et al. 2018

CMC

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Background: Kidney disease is a serious problem that adversely affects human health, but critical knowledge is lacking on how to effectively treat established chronic kidney disease. Mounting evidence from animal and clinical studies has suggested that Vitamin D Re-ceptor (VDR) activation has beneficial effects on various renal diseases.Methods: A structured search of published research literature regarding VDR structure and function, VDR in various renal diseases (e.g., IgA nephropathy, idiopathic nephrotic syndrome, renal cell carcinoma, diabetic nephropathy, lupus nephritis) and therapies targeting VDR was performed for several databases.Result: Included in this study are the results from 177 published research articles. Evidence from these papers indicates that VDR activation is involved in the protection against renal inju-ry in kidney diseases by a variety of mechanisms, including suppression of RAS activation, an-ti-inflammation, inhibiting renal fibrogenesis, restoring mitochondrial function, suppression of autoimmunity and renal cell apoptosis.Conclusion: VDR offers an attractive druggable target for renal diseases. Increasing our under-standing of VDR in the kidney is a fertile area of research and may provide effective weapons in the fight against kidney diseases

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Section: Renoprotective Mechanisms Of Vdrmentioning

confidence: 99%

Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases

Yang

Wang

et al. 2018

CMC

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“…However, long-term exposure of the peritoneal membrane to nonbiocompatible peritoneal dialysis fluid, including high concentrations of glucose and lactate, glucose degradation products (GDPs), and low pH, can result in functional and structural abnormalities of peritoneum, eventually leading to the PD failure [1]. High glucose can lead to inflammation and peritoneal fibrosis (PF) [2], increase the expression of transforming growth factor-β1 (TGF-β1) [3], and stimulate a complex process of peritoneal epithelialmesenchymal transition (EMT) in vivo [4]. EMT of mesothelial cells is an reversible process in which epithelial cells transdifferentiate into cells with mesenchymal characteristics, is widely considered to be a crucial process in fibrosis [5,6].…”

Section: Introductionmentioning

confidence: 99%

Curcumin ameliorates peritoneal fibrosis via inhibition of transforming growth factor-activated kinase 1 (TAK1) pathway in a rat model of peritoneal dialysis

Zhao

Zhang

Shao

et al. 2019

BMC Complement Altern Med

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Background: Peritoneal fibrosis (PF) remains a serious complication of long-term peritoneal dialysis (PD). The goal of this study was to investigate the anti-fibrotic effects of curcumin on the PF response to PD and its' mechanism. Methods: Male Sprague-Dawley rats were infused with 20 mL of 4.25% glucose-based standard PD fluid for 8 consecutive weeks to establish PF model and then divided into five groups: Control, received sham operation and 0.9% physiological saline; PD, received 4.25% standard PD fluid; Curcumin, PD rats injected intraperitoeally with curcumin for 8 weeks at doses of 10, 20 or 40 mg/kg. Masson's staining was performed to evaluate the extent of PF. Peritoneal Equilibration Test (PET) was conducted to assess ultrafiltration volume (UFV) and mass transfer of glucose (MTG), quantitative RT-PCR, and immunohistochemistry or western blotting were performed to measure the expression levels of inflammation and fibrosis-associated factors. We also detected the TGF-β1 in peritoneal fluid by ELISA. Results: Compared with the control group, the PD rats showed decreased UFV (2.54 ± 0.48 to 9.87 ± 0.78 mL, p < 0.05] and increased MTG (18.99 ± 0.86 to 10.85 ± 0.65 mmol/kg, p < 0.05) as well as obvious fibroproliferative response, with markedly increased peritoneal thickness (178.33 ± 4.42 to 25.26 ± 0.32um, p < 0.05) and higher expression of a-SMA, collagen I and TGF-β1. Treatment with curcumin significantly increased UFV, reduced MTG and peritoneal thickness of PD rats. The elevated TGF-β1 in peritoneal fluid of PD rats was significantly decreased by curcumin. It attenuated the increase in protein and mRNA of TGF-β1, α-SMA and collagen I in peritoneum of PD rats. The mRNA expressions of TAK1, JNK and p38, as well as the protein expressions of p-TAK1, p-JNK and p-p38 in peritoneum of PD rats were reduced by curcumin. Conclusions: Present results demonstrate that curcumin showed a protective effect on PD-related PF and suggest an implication of TAK1, p38 and JNK pathway in mediating the benefical effects of curcumin.

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“…Previous studies demonstrated that dencichine could ameliorate kidney injury in induced type II DN via the TGF-β/Smad signaling pathway and 1,25(OH)2D3/VDR could attenuate HG-induced epithelial-mesenchymal transition in human peritoneal mesothelial cells via the TGF-β/Smad3 pathway (13,14). The present study aimed to determine whether the TGF-β/Smad signaling pathway is involved in the regulation of Rg on the HG-affected cell apoptosis and proliferation.…”

Section: Rg Inhibits Hg -Induced Apoptosis and Promotesmentioning

confidence: 89%

Rhein‑8‑O‑β‑D‑glucopyranoside inhibited high glucose‑induced apoptosis of human mesangial cells by regulating the lincRNA ANRIL/let‑7a/TGF‑β1/Smad signaling pathway

Zhang

Liu

2020

Exp Ther Med

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Diabetic nephropathy is one of most frequent complications of diabetes, and is the major cause of end-stage disease in diabetic patients. The present study investigated the roles and mechanisms of Rhein-8-O-β-D-glucopyranoside (Rg) protecting human mesangial cells (HMCs) from high glucose (HG)-induced apoptosis. Using a Cell Counting Kit-8 assay the proliferation of HMCs was analyzed, and flow cytometry was applied to detect apoptosis. The apoptosis-associated protein Bcl-2, caspase-3 and members of the transforming growth factor-β1 (TGF-β1)/Smad signaling pathway were analyzed using a western blotting assay. HG significantly induced HMC apoptosis, and Rg markedly attenuated the HG-induced apoptosis. HG decreased the Bcl-2 expression and increased the caspase-3 expression, and Rg treatment recovered the expressions of Bcl-2 and caspase-3 affected by HG. The underlying mechanisms were further analyzed, and it was demonstrated that HG significantly upregulated the long intervening non-coding RNA (lincRNA) ANRIL expression level, downregulated let-7a expression and activated the TGF-β1/Smad signaling pathway; Rg treatment recovered the expressions of lincRNA ANRIL and let-7a, and inhibited the TGF-β1/Smad signaling pathway in the condition of HG. In conclusion, the present results suggested that Rg attenuated HG-induced apoptosis of HMCs by regulating the lincRNA ANRIL/let-7a/TGF-β1/Smad signaling pathway.

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1,25(OH)2D3/VDR attenuates high glucose-induced epithelial-mesenchymal transition in human peritoneal mesothelial cells via the TGFβ/Smad3 pathway

Cited by 21 publications

References 29 publications

Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases

Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases

Curcumin ameliorates peritoneal fibrosis via inhibition of transforming growth factor-activated kinase 1 (TAK1) pathway in a rat model of peritoneal dialysis

Rhein‑8‑O‑β‑D‑glucopyranoside inhibited high glucose‑induced apoptosis of human mesangial cells by regulating the lincRNA ANRIL/let‑7a/TGF‑β1/Smad signaling pathway

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