Expression of IFN‐induced Transmembrane Protein 1 in Glomerular Endothelial Cells

2020 ◽  
Author(s):  
Shun Hashimoto ◽  
Tadaatsu Imaizumi ◽  
Shojiro Watanabe ◽  
Tomomi Aizawa ◽  
Koji Tsugawa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transmembrane Protein ◽  
Glomerular Endothelial Cells

scholarly journals Hypoxia-induced apoptosis in cultured glomerular endothelial cells: Involvement of mitochondrial pathways

2003 ◽  
Vol 64 (6) ◽  
pp. 2020-2032 ◽  
Author(s):  
Tetsuhiro Tanaka ◽  
Toshio Miyata ◽  
Reiko Inagi ◽  
Kiyoshi Kurokawa ◽  
Stephen Adler ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Glomerular Endothelial Cells ◽  
Induced Apoptosis

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

scholarly journals PR3 and Elastase Alter PAR1 Signaling and Trigger vWF Release via a Calcium-Independent Mechanism from Glomerular Endothelial Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e43916 ◽  
Author(s):  
Samantha P. Tull ◽  
Anne Bevins ◽  
Sahithi Jyothsna Kuravi ◽  
Simon C. Satchell ◽  
Bahjat Al-Ani ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Glomerular Endothelial Cells ◽  
Independent Mechanism

scholarly journals TRPV4-mediated Ca2+ influx is essential to glomerular endothelial inflammation in sepsis associated acute kidney injury

2021 ◽  
Author(s):  
Xia Wang ◽  
Yinhua Wang ◽  
Guo Zhou ◽  
Yi Li ◽  
Huanhuan Huo ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cells ◽  
Cell Injury ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Blood Perfusion ◽  
High Morbidity ◽  
Endothelial Inflammation ◽  
Glomerular Endothelial Cells

Abstract Background Sepsis-associated acute kidney injury (S-AKI) is a frequent complication of critical patients and is associated with high morbidity and mortality. The glomerular endothelial cell injury is the main characteristics during S-AKI. Ca2+ influx is a key step in the establishment of endothelial injury. Transient receptor vanilloid subtype 4 (TRPV4) ion channels are permeable to Ca2+ and are widely expressed in endothelial cells. However, the role of TRPV4 on glomerular endothelial inflammation in S-AKI has remained elusive. Methods Mouse glomerular endothelial cells (MRGEC) were used to test the molecular mechanism of TRPV4 on LPS-induced glomerular endothelial inflammation. The cecal-ligation-and-puncture (CLP) model was established by ligation of cecum with 4-0 suture and punctured with a 21-gauge needle. Then 0.2mL faeces was extruded from the puncture site to trigger peritoneal inflammation. Results In the present study, we found that blocking TRPV4 diminishes LPS-induced cytosolic Ca2+-elevations, which are essential for glomerular endothelial inflammation and barrier function. Furthermore, TRPV4 regulated LPS-induced phosphorylation and translocation of NF-κB and IRF-3 in mouse glomerular endothelial cells (MRGEC). Clamping intracellular Ca2+ mimics the LPS-induce response seen in the absence of TRPV4. In vivo, pharmacological blockade or knock down of TRPV4 reduced the inflammatory response of glomerular endothelial cells, inhibited translocation of NF-κB and IRF-3, increased survival rate and improved renal function in CLP-induced sepsis but without altering renal cortical blood perfusion. Conclusions Taken together, these results suggested that inhibition of TRPV4 ameliorates glomerular endothelial inflammation, kidney dysfunction, and increased mortality via mediating Ca2+ overload and NF-κB/IRF-3 activation. These discoveries may provide novel pharmacological strategies for the treatment of glomerular endothelial dysfunction and kidney injury during endotoxemia, sepsis, and other inflammatory diseases.

scholarly journals ATP‐mediated intercellular calcium wave in renal (juxta)glomerular endothelial cells (GENC)

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Eric Bansal ◽  
Ildiko Toma ◽  
Jung Julie Kang ◽  
Janos Peti‐Peterdi
Keyword(s):  
Endothelial Cells ◽  
Calcium Wave ◽  
Glomerular Endothelial Cells

scholarly journals Shiga Toxin 2 Reduces Complement Inhibitor CD59 Expression on Human Renal Tubular Epithelial and Glomerular Endothelial Cells

2013 ◽  
Vol 81 (8) ◽  
pp. 2678-2685 ◽  
Author(s):  
Silvia Ehrlenbach ◽  
Alejandra Rosales ◽  
Wilfried Posch ◽  
Doris Wilflingseder ◽  
Martin Hermann ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Surface ◽  
Shiga Toxin ◽  
Human Kidney ◽  
Enzyme Linked Immunosorbent Assay ◽  
Content Type ◽  
Protein Levels ◽  
Glomerular Endothelial Cells ◽  
Shiga Toxin 2 ◽  
Renal Tubular

ABSTRACTInfections with enterohemorrhagicEscherichia coli(EHEC) are a primary cause of hemolytic-uremic syndrome (HUS). Recently, Shiga toxin 2 (Stx2), the major virulence factor of EHEC, was reported to interact with complement, implying that the latter is involved in the pathogenesis of EHEC-induced HUS. The aim of the present study was to investigate the effect of Stx2 on the expression of membrane-bound complement regulators CD46, CD55, and CD59 on proximal tubular epithelial (HK-2) and glomerular endothelial (GEnC) cells derived from human kidney cells that are involved in HUS. Incubation with Stx2 did not influence the amount of CD46 or CD55 on the surface of HK-2 and GEnC cells, as determined by fluorescence-activated cell sorter analysis. In contrast, CD59 was significantly reduced by half on GEnC cells, but the reduction on HK-2 cells was less pronounced. With increasing amounts of Stx2, reduction of CD59 also reached significance in HK-2 cells. Enzyme-linked immunosorbent assay analyses showed that CD59 was not present in the supernatant of Stx2-treated cells, implying that CD59 reduction was not caused by cleavage from the cell surface. In fact, reverse transcription-quantitative PCR analyses showed downregulation of CD59 mRNA as the likely reason for CD59 cell surface reduction. In addition, a significant increase in terminal complement complex deposition on HK-2 cells was observed after treatment with Stx2, as a possible consequence of CD59 downregulation. In summary, Stx2 downregulates CD59 mRNA and protein levels on tubular epithelial and glomerular endothelial cells, and this downregulation likely contributes to complement activation and kidney destruction in EHEC-associated HUS.

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