scholarly journals Sitagliptin protects renal glomerular endothelial cells against high glucose-induced dysfunction and injury

Bioengineered ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 655-666
Author(s):  
Liang Xu ◽  
Fengmin Shao
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Glomerular Endothelial Cells

Activation of general control nonderepressible 2 kinase protects human glomerular endothelial cells from harmful high-glucose-induced molecular pathways

2016 ◽  
Vol 48 (10) ◽  
pp. 1731-1739 ◽  
Author(s):  
Theodoros Eleftheriadis ◽  
Konstantina Tsogka ◽  
Georgios Pissas ◽  
Georgia Antoniadi ◽  
Vassilios Liakopoulos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Molecular Pathways ◽  
General Control ◽  
Glomerular Endothelial Cells ◽  
Human Glomerular Endothelial Cells

Sodium butyrate alleviates high-glucose-induced renal glomerular endothelial cells damage via inhibiting pyroptosis

2019 ◽  
Vol 75 ◽  
pp. 105832 ◽  
Author(s):  
Junling Gu ◽  
Wei Huang ◽  
Wenqian Zhang ◽  
Tingting Zhao ◽  
Chenlin Gao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Sodium Butyrate ◽  
High Glucose ◽  
Glomerular Endothelial Cells

scholarly journals Attenuation of Glomerular Endothelial Cells from High Glucose-Induced Injury by Blockade of MAD2B

2015 ◽  
Vol 35 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Yu-Mei Wang ◽  
Yu Hao ◽  
Xian-Fang Meng ◽  
Fang-Fang He ◽  
Shan Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
High Glucose ◽  
Cell Monolayer ◽  
No Production ◽  
Protein Levels ◽  
Glomerular Endothelial Cells ◽  
Monolayer Permeability ◽  
Glucose Treatment ◽  
In Cells

Background/Aims: To assess the role of mitotic arrest-deficient 2-like protein 2 (MAD2B) in high glucose-induced injury in mouse glomerular endothelial cells (GEnCs). Methods: GEnCs were cultured in vitro, and MAD2B protein levels were measured by Western blot in cells stimulated with high glucose (30 mM) for various periods of time. MAD2B and scrambled shRNA were introduced into GEnCs by liposomal transfection. Cell proliferation, apoptosis, nitric oxide (NO) production, and monolayer permeability were then measured in cells grown in the following conditions: control, high glucose treatment, MAD2B shRNA transfection with high glucose treatment, and scrambled shRNA transfection with high glucose treatment. Results: High glucose increased the protein levels of MAD2B in GEnCs. Compared with control cells, apoptosis was increased by high glucose treatment, which was attenuated by transfection with MAD2B shRNA transfection. Cells treated with high glucose produced less NO than control cells, whereas MAD2B shRNA transfection increased NO production. Cell monolayer permeability was enhanced in high glucose treated cells, but MAD2B shRNA transfection reduced permeability. Conclusion: High glucose levels induced the expression of MAD2B in GEnCs, whereas suppressing its expression reduced high glucose-induced endothelial cell apoptosis and high permeability, and promoted cell proliferation and NO production.

scholarly journals The Role of MicroRNA-155 in Glomerular Endothelial Cell Injury of Diabetic Nephropathy

2021 ◽  
Author(s):  
Kaiying He ◽  
Zhan Chen ◽  
Jing Zhao ◽  
Yang He ◽  
Rongrong Deng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
High Glucose ◽  
Cell Injury ◽  
Inflammatory Factors ◽  
Glucose Stimulation ◽  
Endothelial Cell Injury ◽  
Glomerular Endothelial Cells ◽  
Human Glomerular Endothelial Cells

Abstract Objective: To investigate the role of microRNA-155-5p (miR-155-5p) on apoptosis and inflammatory response in human glomerular endothelial cells (HRGEC) cultured with high glucose.Methods: The primary human glomerular endothelial cells (HRGEC) were studied, QPCR, WB , IF were used to detect cell morphology, target gene ETS-1 (ETS-1), downstream factors VCAM-1 and MCP-1, and apoptosis of cells in each group after high glucose stimulation and transfection with miR-155 overexpression or inhibitor.Results:1.The expression of inflammatory factors and apoptosis of HRGEC cells increased under high glucose stimulation.2.The overexpression of miR-155 in HRGEC cells under high glucose stimulation decreased the expression of ETS-1, while the expression of ETS-1 increased when miR-155 was inhibited. These results suggest that miR-155 may be involved in endothelial cell injury by negatively regulating the expression of ETS-1.3.HRGEC cells were transfected with miR-155 mimic and ETS-1 siRNA with high glucose stimulation. The expression of ETS-1 was positively correlated with the expression of downstream factors VCAM-1 and MCP-1. These results suggest that ETS-1 can mediate endothelial cell inflammation by regulating VCAM-1 and MCP-1.

scholarly journals ets1 associates with KMT5A to participate in high glucose-mediated EndMT via upregulation of PFN2 expression in diabetic nephropathy

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Lihong Lu ◽  
Ziwen Zhong ◽  
Jiahui Gu ◽  
Ke Nan ◽  
Minmin Zhu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Diabetic Nephropathy ◽  
High Glucose ◽  
Epithelial To Mesenchymal Transition ◽  
Umbilical Vein ◽  
Human Subjects ◽  
Histone H4 ◽  
Mesenchymal Transition ◽  
Glomerular Endothelial Cells

Abstract Background Diabetic nephropathy (DN) is currently the leading cause of end-stage renal disease globally. The endothelial-to-mesenchymal transition (EndMT) of glomerular endothelial cells has been reported to play a crucial role in DN. As a specific form of epithelial-to-mesenchymal transition, EndMT and epithelial-to-mesenchymal transition may exhibit mutual modulators. Profilin 2 (PFN2) has been reported to participate in epithelial-to-mesenchymal transition. Moreover, ETS proto-oncogene 1 (ets1) and lysine methyltransferase 5A (KMT5A) have been reported to contribute to high glucose-mediated endothelial injury and epithelial-to-mesenchymal transition. In this study, we hypothesize ets1 associates with KMT5A to modulate PFN2 transcription, thus participating in high glucose-mediated EndMT in glomerular endothelial cells. Methods Immunohistochemistry (IHC) was performed to detect protein levels in the kidney tissues and/or aorta tissues of human subjects and rats. Western blot, qPCR and immunofluorescence were performed using human umbilical vein endothelial cells (HUVECs). Chromatin immunoprecipitation (ChIP) assays and dual luciferase assays were performed to assess transcriptional activity. The difference between the groups was compared by two-tailed unpaired t-tests or one-way ANOVAs. Results Our data indicated that vimentin, αSMA, S100A4 and PFN2 levels were increased, and CD31 levels were reduced in glomerular endothelial cells of DN patients and rats. Our cell experiments showed that high glucose induced EndMT by augmenting PFN2 expression in HUVECs. Moreover, high glucose increased ets1 expression. si-ets1 suppressed high glucose-induced PFN2 levels and EndMT. ets1 overexpression-mediated EndMT was reversed by si-PFN2. Furthermore, ets1 was determined to associate with KMT5A. High glucose attenuated KMT5A levels and histone H4 lysine 20 methylation (H4K20me1), one of the downstream targets of KMT5A. KMT5A upregulation suppressed high glucose-induced PFN2 levels and EndMT. sh-KMT5A-mediated EndMT was counteracted by si-PFN2. Furthermore, H4K20me1 and ets1 occupied the PFN2 promoter region. sh-KMT5A cooperated with ets1 overexpression to activate PFN2 promoter activity. Our in vivo study demonstrated that KMT5A was reduced, while ets1 was augmented, in glomerular endothelial cells of DN patients and rats. Conclusions The present study indicated that ets1 cooperated with KMT5A to transcribe PFN2, thus contributing to hyperglycemia-induced EndMT in the glomerular endothelial cells of DN patients and rats. Trial registration ChiCTR, ChiCTR2000029425. 2020/1/31, http://www.chictr.org.cn/showproj.aspx?proj=48548

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