Effect of High Glucose on Superoxide in Human Mesangial Cells: Role of Angiotensin II

2005 ◽  
Vol 100 (1) ◽  
pp. 46-53 ◽  
Author(s):  
David J. Leehey ◽  
Majd A. Isreb ◽  
Sonja Marcic ◽  
Ashok K. Singh ◽  
Rekha Singh
Keyword(s):  
Angiotensin Ii ◽  
High Glucose ◽  
Mesangial Cells ◽  
Human Mesangial Cells

Role of aldose reductase in the high glucose induced expression of fibronectin in human mesangial cells

2009 ◽  
Vol 37 (6) ◽  
pp. 3017-3021 ◽  
Author(s):  
Ping Huang ◽  
Yuejuan Zhang ◽  
Tao Jiang ◽  
Wenjiao Zeng ◽  
Nong Zhang
Keyword(s):  
Aldose Reductase ◽  
High Glucose ◽  
Mesangial Cells ◽  
Induced Expression ◽  
Human Mesangial Cells

Regulation of Glucose Uptake in Mesangial Cells Stimulated by High Glucose: Role of Angiotensin II and Insulin

2009 ◽  
Vol 234 (9) ◽  
pp. 1095-1101 ◽  
Author(s):  
Carine P. Arnoni ◽  
Carla Lima ◽  
Priscila C. Cristovam ◽  
Edgar Maquigussa ◽  
Daniela B. Vidotti ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Glucose Uptake ◽  
High Glucose ◽  
Glucose Transporter ◽  
Mesangial Cells ◽  
Dependent Manner ◽  
Beneficial Effects ◽  
Fibronectin Expression ◽  
Insulin Dependent

Mesangial cells (MCs) play a central role in the pathogenesis of diabetic nephropathy (DN). MC dysfunction arises from excessive glucose uptake through insulin-independent glucose transporter (GLUT1). The role of the insulin-dependent transporter (GLUT4) remains unknown. This study evaluated the effect of high glucose on GLUT1, GLUT4, and fibronectin expression levels. Glucose uptake was determined in the absence and presence of insulin. Angiotensin II has been implicated as a mediator of MC abnormalities in DN, and its effects on the GLUTs expression were evaluated in the presence of losartan. MCs were exposed to normal (NG, 10 m M) or high (HG, 30 m M) glucose for 1, 4, 12, 24, and 72 hrs. Glucose uptake was elevated from 1 hr up to 24 hrs of HG, but returned to NG levels after 72 hrs. HG induced an early (1-, 4-, and 12-hrs) rise in GLUT1 expression, returning to NG levels after 72 hrs, whereas GLUT4 was overexpressed at later timepoints (24 and 72 hrs). HG during 4 hrs induced a 40% rise in glucose uptake, which was unaffected by insulin. In contrast, after 72 hrs, glucose uptake was increased by 50%, only under insulin stimulus. Losartan blunted the effects of HG on GLUT1, GLUT4, and fibronectin expression and on glucose uptake. Results suggest that MCs can be highly susceptible to the HG environment since they uptake glucose in both an insulin-independent and insulin-dependent manner. The beneficial effects of angiotensin II inhibition in DN may also involve a decrease in the rate of glucose uptake by MCs.

scholarly journals LncRNA NEAT1 Promotes High Glucose-Induced Mesangial Cell Hypertrophy by Targeting miR-222-3p/CDKN1B Axis

2021 ◽  
Vol 7 ◽  
Author(s):  
Lin Liao ◽  
Jie Chen ◽  
Chuanfu Zhang ◽  
Yue Guo ◽  
Weiwei Liu ◽  
...  
Keyword(s):  
High Glucose ◽  
Noncoding Rna ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Morphological Alteration ◽  
Glomerular Hypertrophy ◽  
Cell Hypertrophy ◽  
Rna Immunoprecipitation ◽  
Lncrna Neat1

Glomerular hypertrophy is an early morphological alteration in diabetic nephropathy. Cyclin-Dependent Kinases have been shown to be required for high glucose (HG)-induced hypertrophy; however, the upstream regulators of CDKN1B in glomerular hypertrophy remain unclear. Herein we describe a novel pathway in which Long noncoding RNA (lncRNA) NEAT1 regulates the progression of mesangial cell hypertrophy via a competing endogenous RNA (ceRNA) mechanism. Real-time PCR was performed to detect the relative NEAT1 and miR-222-3p expressions and further confirmed the relationship between NEAT1 and miR-222-3p. Cell cycle was evaluated by flow cytometry. The related mechanisms were explored by Western blot, RNA immunoprecipitation and chromatin immunoprecipitation assay. We show that NEAT1 forms double stranded RNA (dsRNA) with miR-222-3p, thus limiting miR-222-3p’s binding with CDKN1B. This release of CDKN1B mRNA leads to elevated CDKN1B protein expression, resulting in hypertrophy. In addition, we demonstrated that STAT3 which is activated by HG induces the transcription of NEAT1 by binding to its promoter. Our findings underscore an unexpected role of lncRNAs on gene regulation and introduce a new mode of proliferation regulation in mesangial cells.

Mesangial cells express PDGF mRNAs and proliferate in response to PDGF

1988 ◽  
Vol 255 (4) ◽  
pp. F674-F684 ◽  
Author(s):  
P. J. Shultz ◽  
P. E. DiCorleto ◽  
B. J. Silver ◽  
H. E. Abboud
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Northern Blot Analysis ◽  
Mesangial Cells ◽  
Glomerular Mesangial Cells ◽  
Human Mesangial Cells ◽  
Human Foreskin Fibroblasts ◽  
Human Glomerular Mesangial Cells ◽  
Paracrine Growth Factor

Platelet-derived growth factor (PDGF) is a potent mitogen for cells of mesenchymal origin and is released and/or synthesized by platelets, macrophages, endothelial cells, and rat mesangial cells. In the present investigation, we found that human glomerular mesangial cells in culture release a PDGF-like protein which competes for 125I-PDGF binding to human foreskin fibroblasts and is mitogenic for these fibroblasts. The competing and to a lesser extent the mitogenic activities present in the conditioned medium are partially recognized by an anti-PDGF antibody. Northern blot analysis of poly(A)+ RNA from human mesangial cells demonstrates the expression of both PDGF A- and B-chain mRNAs. PDGF also binds to mesangial cells in a specific manner and stimulates DNA synthesis and cell proliferation. These data suggest that a PDGF-like protein secreted by mesangial cells or released from platelets, monocytes, or endothelial cells during glomerular inflammation may function as an autocrine or a paracrine growth factor for these cells. The biological role of PDGF in mediating proliferative and other inflammatory events in the glomerulus remains to be identified.

Dexamethasone upregulates ANP C-receptor protein in human mesangial cells without affecting mRNA

1996 ◽  
Vol 270 (3) ◽  
pp. F440-F446 ◽  
Author(s):  
N. Ardaillou ◽  
V. Blaise ◽  
S. Placier ◽  
F. Amestoy ◽  
R. Ardaillou
Keyword(s):  
Glucocorticoid Receptor ◽  
Natriuretic Peptide ◽  
Mesangial Cells ◽  
Receptor Protein ◽  
C Protein ◽  
Human Mesangial Cells ◽  
Receptor Inhibition ◽  
Target Sites ◽  
Dissociation Constant Kd

The objective of this study was to examine the role of dexamethasone on the expression of natriuretic peptide B-type and C-type receptors (ANPR-B and ANPR-C) in cultured human mesangial cells, which only possess these two subtypes. Dexamethasone caused concentration- and time-dependent increases in 125I-labeled ANP binding, which were prevented by glucocorticoid receptor inhibition with RU-38486. A lag time of 24 h and a concentration of dexamethasone of at least 1 nmol/l were necessary for this effect to occur. Dexamethasone-induced upregulation of 125I-ANP binding resulted from increased receptor density. No change in dissociation constant (Kd) was observed. Only ANPR-C were affected by dexamethasone. Indeed, dexamethasone did not modify C-type natriuretic peptide (i.e., CNP)-dependent cGMP production by mesangial cells. Moreover, dexamethasone upregulated ANPR-C protein expression as shown by Western blot analysis and by an increase in ANPR-C immunoreactivity at the cell surface. In contrast, dexamethasone did not modify ANPR-C mRNA expression. In conclusion, glucocorticoids increase ANPR-C density on mesangial cells through a mechanism implying, successively, interaction with the glucocorticoid receptor and increase of ANPR-C protein synthesis at a posttranscriptional stage. Thus dexamethasone may influence availability of natriuretic peptides at their glomerular target sites.

scholarly journals High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells

Renal Failure ◽  
2019 ◽  
Vol 41 (1) ◽  
pp. 762-769
Author(s):  
Fumeng Huang ◽  
Yuanxu Guo ◽  
Li Wang ◽  
Lanmei Jing ◽  
Zhao Chen ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
High Glucose ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Selenoprotein S ◽  
Tgf Β1

scholarly journals High glucose and hyperosmolality stimulate hepatocyte growth factor secretion from cultured human mesangial cells

Diabetologia ◽  
1994 ◽  
Vol 37 (5) ◽  
pp. 533-535 ◽  
Author(s):  
J. J. Couper ◽  
A. Ferrante ◽  
K. D. Littleford ◽  
R. T. L. Couper ◽  
T. Nakamura
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
High Glucose ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Hepatocyte Growth ◽  
Factor Secretion ◽  
Growth Factor Secretion
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