Transforming Growth Factor-Beta-1 Latency-Associated Peptide and Soluble Betaglycan Prevent a Glucose-Induced Increase in Fibronectin Production in Cultured Human Mesangial Cells

Nephron ◽  
2002 ◽  
Vol 91 (4) ◽  
pp. 606-611 ◽  
Author(s):  
Kayoko Nomura ◽  
Hisaya Tada ◽  
Koji Kuboki ◽  
Toshiki Inokuchi
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Growth Factor Beta

scholarly journals Transforming growth factor beta regulates cyclooxygenase-2 in glomerular mesangial cells

2006 ◽  
Vol 69 (9) ◽  
pp. 1578-1585 ◽  
Author(s):  
P. Harding ◽  
L. Balasubramanian ◽  
J. Swegan ◽  
A. Stevens ◽  
W.F. Glass
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Cyclooxygenase 2 ◽  
Glomerular Mesangial Cells ◽  
Growth Factor Beta

scholarly journals Interactions between glomerular mesangial cells, cytokines, and extracellular matrix.

1992 ◽  
Vol 2 (10) ◽  
pp. S126
Author(s):  
R B Sterzel ◽  
E Schulze-Lohoff ◽  
M Weber ◽  
S L Goodman
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Platelet Derived Growth Factor ◽  
Glomerular Mesangial Cells ◽  
Cell Replication ◽  
Glomerular Cell ◽  
Growth Factor Beta

This brief overview summarizes recent information on the interactions of glomerular mesangial cells (MC) with soluble cytokines and nonsoluble extracellular matrix (ECM). The presently available knowledge stems largely from glomerular cell culture studies and from experimental work with laboratory animals. ECM production by MC appears to be regulated primarily by the paracrine or autocrine effects of cytokines, such as interleukin 1, platelet-derived growth factor, and transforming growth factor beta. However, ECM itself also affects the behavior of cultured MC, e.g., with regard to cell replication and the production of ECM components and other proteins. At present, little is known about the recognition of ECM and cytokines by MC that allows these interactions to take place. First results indicate that MC, like other cell types, possess surface proteins belonging to the beta 1 integrin family, which serve as specific receptors for ECM molecules. Receptors for the cytokines platelet-derived growth factor, insulin-like growth factor 1, epidermal growth factor, and transforming growth factor beta have also been demonstrated on MC. The expression of various receptors on MC appears to be affected by the ECM substratum. Thus, it is becoming apparent that mesangial ECM is not only important as a mechanical scaffold of the glomerular capillary tuft but that it also contains and conveys information relevant for the regulation of the MC phenotype, e.g., by modulating the MC response to cytokines. The available evidence suggests that alterations of ECM composition in glomerular disease can directly or indirectly affect MC behavior, e.g., by promoting cell replication and further accumulation of ECM, eventually resulting in progressive mesangial and glomerular sclerosis.

scholarly journals Differential effects of angiotensin II and transforming growth factor beta on the production of heparan sulfate proteoglycan by mesangial cells in vitro.

1996 ◽  
Vol 7 (7) ◽  
pp. 1015-1023
Author(s):  
N F van Det ◽  
J T Tamsma ◽  
J van den Born ◽  
N A Verhagen ◽  
L P van den Heuvel ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Heparan Sulfate ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Heparan Sulfate Proteoglycan ◽  
Sulfate Proteoglycan ◽  
Tgf Beta ◽  
Growth Factor Beta

This study approaches the question of whether angiotensin II (AngII) and transforming growth factor beta (TGF-beta) are important mediators for mesangial heparan sulfate proteoglycan (HSPG) production. This might explain the beneficial effects of angiotensin-converting enzyme inhibitors observed in several kidney diseases independent from their hemodynamic effects. Metabolic-labeling studies revealed that AngII induced a decrease of HSPG synthesis with decreases in N-sulfation of the glycosaminoglycan side chains. ELISA measurements with a heparan sulfate (HS)-specific monoclonal antibody confirmed that AngII decreased HS production. AngII increased TGF-beta production in a dose-dependent fashion. Specific mRNA for the large basement membrane HSPG (perlecan) decreased, whereas mRNA for TGF-beta increased after incubation with AngII. Blockade of the Subtype 1 Ang-II receptor (ATR1) reversed both the effects of AngII on HSPG and TGF-beta production. Coincubation of the mesangial cells with neutralizing antibodies against TGF-beta significantly reduced the production of HS as compared with control and AngII. These results indicate that the decrease in HS synthesis induced by AngII is not mediated by an increase in TGF-beta, but on the contrary, the increase in TGF-beta partially counteracts the inhibition of HS production by AngII. Considering the important role of HSPG in maintaining the glomerular charge barrier, cell proliferation, and matrix interaction, downregulation of the production of this molecule by increased local AngII concentrations could have important consequences, such as albuminuria and matrix expansion.

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