scholarly journals Laminin α1 Regulates Age-Related Mesangial Cell Proliferation and Mesangial Matrix Accumulation through the TGF-β Pathway

2014 ◽  
Vol 184 (6) ◽  
pp. 1683-1694 ◽  
Author(s):  
Liang Ning ◽  
Hidetake Kurihara ◽  
Susana de Vega ◽  
Naoki Ichikawa-Tomikawa ◽  
Zhuo Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Matrix ◽  
Age Related ◽  
Mesangial Cell Proliferation ◽  
Matrix Accumulation

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.

scholarly journals C-type natriuretic peptide inhibits mesangial cell proliferation and matrix accumulation in vivo

1998 ◽  
Vol 53 (5) ◽  
pp. 1143-1151 ◽  
Author(s):  
Sima Canaan-Kühl ◽  
Tammo Ostendorf ◽  
Kerstin Zander ◽  
Karl-Martin Koch ◽  
Jürgen Floege
Keyword(s):  
Cell Proliferation ◽  
Natriuretic Peptide ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Matrix Accumulation

Gene expression profiling reveals role for EGF-family ligands in mesangial cell proliferation

2002 ◽  
Vol 283 (5) ◽  
pp. F1151-F1159 ◽  
Author(s):  
Rangnath Mishra ◽  
Patrick Leahy ◽  
Michael S. Simonson
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Cell Growth ◽  
Mesangial Cell ◽  
Tissue Injury ◽  
Expression Patterns ◽  
Mesangial Cell Proliferation ◽  
Egf Family ◽  
Matrix Accumulation

Control of mesangial cell growth and matrix accumulation is critical for normal development of the glomerular tuft and progression of glomerular injury, but the genes that control mesangial cell growth are not well understood. We used high-density oligonucleotide microarrays to analyze gene expression in well-differentiated human mesangial cells treated with serum to stimulate proliferation. Parallel measurement of >12,000 genes and expressed sequence tags identified 5,806 mRNA transcripts in quiescent, unstimulated cells and 609 genes significantly induced or repressed by serum. Functional classification of serum-regulated genes revealed many genes not directly related to cell cycle progression that, instead, might control renal hemodynamics and glomerular filtration or cause tissue injury, leukocyte exudation, matrix accumulation, and fibrosis. Hierarchical cluster analysis defined sets of coregulated genes with similar functions and identified networks of proinflammatory genes with similar expression patterns. Pathway analysis of the gene expression profile suggested an autocrine role in mesangial cell proliferation for three growth factors in the epidermal growth factor (EGF) family: heparin-binding EGF-like growth factor, amphiregulin, and epiregulin. A functional role for EGF receptor (EGFR) activation was confirmed by blocking serum-induced proliferation with an EGFR-selective kinase inhibitor and a specific EGFR-neutralizing antibody. Taken together, these results suggest a role for EGFR signaling in control of mesangial cell growth in response to serum.

scholarly journals Hypertriglyceridemia Is Associated with More Severe Histological Glomerulosclerosis in IgA Nephropathy

2021 ◽  
Vol 10 (18) ◽  
pp. 4236
Author(s):  
Won Jung Choi ◽  
Yu Ah Hong ◽  
Ji Won Min ◽  
Eun Sil Koh ◽  
Hyung Duk Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Risk Factor ◽  
Iga Nephropathy ◽  
Mesangial Cell ◽  
Significant Risk ◽  
Density Lipoprotein ◽  
Significant Risk Factor ◽  
Mesangial Matrix ◽  
Mesangial Cell Proliferation ◽  
Matrix Expansion

IgA nephropathy (IgAN) is a globally well-known primary glomerular nephropathy. Hypertriglyceridemia (HTG) is one factor contributing to atherosclerosis and is a common complication of renal failure. HTG is a significant risk factor for decreased renal function in patients with IgAN. We evaluated the association of HTG with the histopathological features of IgAN patients. A total of 480 patients diagnosed with IgAN via kidney biopsy from eight university hospitals affiliated with the College of Medicine of the Catholic University of Korea were included in the final cohort. Pathological features were evaluated by eight expert pathologists with hospital consensus. HTG was defined as a serum triglyceride (TG) level of ≥150 mg/dL. In the study population analysis, the HTG group was older, with more males; higher body mass index (BMI), low-density lipoprotein cholesterol (LDL-C) and spot urine protein ratio; and lower estimated glomerular filtration rate (eGFR). In the lipid profile analysis, eGFR was negatively correlated with TGs/ high-density lipoprotein cholesterol (HDL) and triglyceride-glucose index (TyG). Proteinuria positively correlated with TGs/HDL, non-HDL/HDL, LDL/HDL, TyG, TGs and LDL. The percentages of global sclerosis (GS), segmental sclerosis (SS) and capsular adhesion (CA), and the scores for mesangial matrix expansion (MME) and mesangial cell proliferation (MCP), were more elevated in the HTG group compared to the normal TG group. Multivariable linear regression analysis showed that the percentages of global sclerosis, segmental sclerosis and capsular adhesion, as well as the scores for mesangial matrix expansion and mesangial cell proliferation, were positively associated with TG level. In binary logistic regression, the HTG group showed a higher risk for global sclerosis and segmental sclerosis. In conclusion, HTG is a significant risk factor for glomerulosclerosis in IgAN.

scholarly journals Expression of Megsin mRNA, a Novel Mesangium-Predominant Gene, in the Renal Tissues of Various Glomerular Diseases

1999 ◽  
Vol 10 (12) ◽  
pp. 2606-2613
Author(s):  
DAISUKE SUZUKI ◽  
TOSHIO MIYATA ◽  
MASAOMI NANGAKU ◽  
HIDEO TAKANO ◽  
NOBORU SAOTOME ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Periodic Acid ◽  
Cell Number ◽  
Mesangial Matrix ◽  
Periodic Acid Schiff ◽  
Glomerular Diseases ◽  
Mesangial Cell Proliferation ◽  
Matrix Expansion

Abstract. Mesangial cells play an important role in maintaining a structure and function of the glomerulus and in the pathogenesis of glomerular diseases. Recently, we discovered a new mesangium-predominant gene termed “megsin.” Megsin is a novel protein that belongs to the serine protease inhibitor (serpin) superfamily. To elucidate the pathophysiologic role of megsin in the kidney, the expression and localization of megsin mRNA in renal tissues of patients with IgA nephropathy (IgA-N), diabetic nephropathy (DN), minimal change nephrotic syndrome (MCNS), membranous nephropathy (MN), and normal human kidney (NHK) was evaluated by in situ hybridization using digoxigenin-labeled oligonucleotide. Individual cells positive for megsin mRNA were observed only in glomeruli in all renal tissues. Their localization coincided with those of mesangial cells. The percentage of positive cells for megsin mRNA in total glomerular cells was significantly greater in IgA-N than in MCNS, MN, and NHK. It was also significantly greater in DN than in MCNS and NHK. In IgA-N, the percentage of megsin mRNA-positive cells was greater in tissues from those with mesangial cell proliferation and slightly mesangial matrix expansion (periodic acid-Schiff-positive area in the total glomerulus area, <30%; cell number in mesangial matrix area, >30; assessed in cross-sections through their vascular poles) than in tissues from those with severe mesangial matrix expansion (periodic acid-Schiff-positive area in total glomerulus area, >30%; cell number in mesangial matrix area, <30). In conclusion, megsin mRNA was predominantly expressed in glomerular mesangial cells in all renal tissues. The expression of megsin mRNA was upregulated in IgA-N and DN, both of which are diseases accompanied with mesangial cell proliferation and/or mesangial matrix expansion. These data suggest a link of megsin expression to the pathogenesis of IgA-N and DN, two major causes of end-stage renal failure.

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