Morphine Modulates Mesangial Immunoglobulin G Uptake in Rats with Antithymocyte Serum-Induced Mesangial Cell Injury

Nephron ◽  
1996 ◽  
Vol 74 (1) ◽  
pp. 197-203 ◽  
Author(s):  
Pravin C. Singhal ◽  
Calvin Q. Pan ◽  
Sushil Sagar ◽  
E. Valderrama ◽  
Rolf A.K. Stahl
Keyword(s):  
Immunoglobulin G ◽  
Cell Injury ◽  
Mesangial Cell

S1P modulator FTY720 limits matrix expansion in acute anti-thy1 mesangioproliferative glomerulonephritis

2007 ◽  
Vol 292 (6) ◽  
pp. F1761-F1770 ◽  
Author(s):  
Sebastian Martini ◽  
Stephanie Krämer ◽  
Tanja Loof ◽  
Yingrui Wang-Rosenke ◽  
Ute Daig ◽  
...  
Keyword(s):  
Protein Expression ◽  
Blood Lymphocyte ◽  
Matrix Protein ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Staining Intensity ◽  
Beneficial Effects ◽  
Collagen Iii ◽  
Mesangioproliferative Glomerulonephritis ◽  
Matrix Expansion

FTY720 is a novel immune modulator whose primary action is blood lymphocyte depletion through interaction with sphingosine-1-phosphate (S1P) receptors. The present study analyzes the effect of FTY720 on both the early mesangial cell injury and the subsequent matrix expansion phase of experimental mesangioproliferative glomerulonephritis. Disease was induced by injection of OX-7 anti-thy1 antibody into male Wistar rats. In both protocols, FTY720 administration (0.3 mg/kg body wt) resulted in a selective and very marked reduction in blood lymphocyte count. In the injury experiment, the S1P receptor modulator was given starting 5 days before and continued until 1 day after antibody injection. FTY720 did not significantly affect the degree of anti-thy1-induced mesangial cell lysis and glomerular-inducible nitric oxide production. In the matrix expansion experiment, FTY720 treatment was started 1 day after antibody injection and continued until day 7. In this protocol, the S1P modulator reduced proteinuria, histological matrix expansion, and glomerular protein expression of TGF-β1, fibronectin, and PAI-1. Glomerular collagen III staining intensity was decreased. FTY720 reduced markedly glomerular lymphocyte number per cross section and to a lesser degree macrophage infiltration. In conclusion, FTY720 significantly limits TGF-β1 overexpression and matrix protein expression following induction of acute anti-thy glomerulonephritis, involving reductions in blood and glomerular lymphocyte numbers. The results suggest that lymphocytes actively contribute to matrix expansion in experimental mesangioproliferative glomerulonephritis. Our study expands on findings on FTY720's beneficial effects on tubulointerstitial and functional disease progression previously reported in anti-thy1-induced chronic glomerulosclerosis.

Mass spectrometry-based circulating IgA1 complexes screening driven identification of IgA-alpha-1-microglobulin complex in IgA nephropathy

2020 ◽  
Author(s):  
Boyang Xu ◽  
Li Zhu ◽  
Qingsong Wang ◽  
Yanfeng Zhao ◽  
Meng Jia ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Iga Nephropathy ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Independent Population ◽  
Tubulointerstitial Lesions ◽  
Noninvasive Biomarker

Abstract Background IgA nephropathy (IgAN) is characterized by predominant IgA deposition in the glomerular mesangium. Previous studies proved that renal-deposited IgA in IgAN came from circulating IgA1-containing complexes (CICs). Methods To explore the composition of CICs in IgAN, we isolated CICs from IgAN patients and healthy controls, and then quantitatively analyzed them by mass spectrometry. Meanwhile, the isolated CICs were used to treat human mesangial cells to monitor mesangial cell injury. Taken together the proteins content and injury effects, the key constituent in CICs was identified. Then, the circulating levels of identified key constituent-IgA complex were detected in an independent population by an in-house-developed ELISA. Results By comparing the proteins of CICs between IgAN patients and controls, we found that 14 proteins showed significantly different levels. Among them, alpha-1-microglobulin content in CICs was associated with not only in vitro mesangial cell proliferation and MCP-1 secretion but also in vivo eGFR levels and tubulointerstitial lesions in IgAN patients. Moreover, we found alpha-1-microglobulin was prone to bind aberrant glycosylated IgA1. Additionally, an elevated circulating IgA-alpha-1-microglobulin complex levels were detected in an independent IgAN population, and IgA-alpha-1-microglobulin complex levels were correlated with hypertension, eGFR levels and Oxford-T scores in these IgAN patients. Conclusions Our results suggest that the IgA-alpha-1-microglobulin complex is an important constituent in CICs, and that circulating IgA-alpha-1-microglobulin complex detection might serve as a potential noninvasive biomarker detection method for IgAN.

LncRNA NEAT1 accelerates renal mesangial cell injury via modulating the miR-146b/TRAF6/NF-κB axis in lupus nephritis

2020 ◽  
Vol 382 (3) ◽  
pp. 627-638 ◽  
Author(s):  
Li-Hua Zhang ◽  
Bin Xiao ◽  
Miao Zhong ◽  
Qiao Li ◽  
Jian-Ying Chen ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Lncrna Neat1

scholarly journals Acteoside relieves mesangial cell injury by regulating Th22 cell chemotaxis and proliferation in IgA nephropathy

Renal Failure ◽  
2018 ◽  
Vol 40 (1) ◽  
pp. 364-370 ◽  
Author(s):  
Lu Gan ◽  
Xiaozhao Li ◽  
Mengyuan Zhu ◽  
Chen Chen ◽  
Huimin Luo ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Cell Chemotaxis

scholarly journals MicroRNA-27a Induces Mesangial Cell Injury by Targeting of PPARγ and its In Vivo Knockdown Prevents Progression of Diabetic Nephropathy

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Lina Wu ◽  
Qingzhu Wang ◽  
Feng Guo ◽  
Xiaojun Ma ◽  
Hongfei Ji ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Cell Injury ◽  
Mesangial Cell

scholarly journals Ursolic Acid Attenuates Diabetic Mesangial Cell Injury through the Up-Regulation of Autophagy via miRNA-21/PTEN/Akt/mTOR Suppression

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0117400 ◽  
Author(s):  
Xinxing Lu ◽  
Qiuling Fan ◽  
Li Xu ◽  
Lin Li ◽  
Yuan Yue ◽  
...  
Keyword(s):  
Ursolic Acid ◽  
Cell Injury ◽  
Mesangial Cell

scholarly journals Chemoattractants provoke monocyte adhesion to human mesangial cells and mesangial cell injury

1992 ◽  
Vol 42 (2) ◽  
pp. 480-487 ◽  
Author(s):  
Hugh R. Brady ◽  
Mark D. Denton ◽  
Wladimiro Jimenez ◽  
Shoichiro Takata ◽  
Deborah Palliser ◽  
...  
Keyword(s):  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Monocyte Adhesion ◽  
Human Mesangial Cells

scholarly journals Immune-mediated mesangial cell injury—Biosynthesis and function of prostanoids

1990 ◽  
Vol 38 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Rolf A.K. Stahl ◽  
Friedrich Thaiss ◽  
Sabine Kahf ◽  
Wilhelm Schoeppe ◽  
Udo M. Helmchen
Keyword(s):  
Cell Injury ◽  
Mesangial Cell ◽  
Immune Mediated ◽  
And Function

scholarly journals Heparin decreases mesangial matrix accumulation after selective antibody-induced mesangial cell injury.

1992 ◽  
Vol 3 (4) ◽  
pp. 921-929
Author(s):  
W W Tang ◽  
C B Wilson
Keyword(s):  
Cell Proliferation ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Chronic Administration ◽  
Glomerular Mesangial Cells ◽  
Mesangial Matrix ◽  
Beneficial Effects ◽  
Mesangial Cell Proliferation ◽  
Matrix Accumulation

Anti-rat thymocyte antibody-induced injury of glomerular mesangial cells is characterized initially by lysis (1 h) and is followed by proliferation (beginning at 3 to 4 days), with resolution that can include a focal increase in mesangial matrix (by 28 days). Chronic administration (every 12 h) of heparin (anticoagulant or nonanticoagulant) resulted in a decrease in antibody-induced mesangial cell proliferation, which, in turn, was associated with a decrease in the size and number of areas of focal mesangial matrix increase. The effect could not be attributed to the effect of heparin on complement, to alterations in the small numbers of la-positive cells that characterize the lesion, or to binding of antibody to glomeruli. The beneficial effects of heparin in reducing mesangial cell proliferation, with a subsequent reduction in matrix increase, suggest that mesangial cell responses are a major element in the development of at least some forms of glomerulosclerosis. The possible mechanisms by which these effects of heparin may be achieved are discussed.

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