scholarly journals Dact1, a Wnt-Pathway Inhibitor, Mediates Human Mesangial Cell TGF-β1-Induced Apoptosis

2017 ◽  
Vol 232 (8) ◽  
pp. 2104-2111 ◽  
Author(s):  
Daniele Pereira Jardim ◽  
Paula Cristina Eiras Poço ◽  
Alexandre Holthausen Campos
Keyword(s):  
Wnt Pathway ◽  
Mesangial Cell ◽  
Human Mesangial Cell ◽  
Induced Apoptosis ◽  
Tgf Β1

Local production of TGF β1 inhibits cerebral edema, enhances TNF-α induced apoptosis and improves survival in a murine glioma model

1998 ◽  
Vol 86 (1) ◽  
pp. 46-52 ◽  
Author(s):  
David M Ashley ◽  
John H Sampson ◽  
Gary E Archer ◽  
Laura P Hale ◽  
Darell D Bigner
Keyword(s):  
Cerebral Edema ◽  
Local Production ◽  
Tnf Α ◽  
Glioma Model ◽  
Induced Apoptosis ◽  
Tgf Β1 ◽  
Murine Glioma

scholarly journals Expression of extracellular matrix molecules in human mesangial cells in response to prolonged hyperglycaemia

1996 ◽  
Vol 316 (3) ◽  
pp. 985-992 ◽  
Author(s):  
Nadia Abdel WAHAB ◽  
Katherine HARPER ◽  
Roger M. MASON
Keyword(s):  
Cell Cultures ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Dermal Fibroblasts ◽  
Rt Pcr ◽  
Collagen Types ◽  
Human Mesangial Cells ◽  
Core Proteins ◽  
Cell Layers ◽  
Tgf Β1

Post-mitotic cultures of human mesangial cells were maintained in media containing 4–30 mM D-glucose for up to 28 days. Changes in mRNA and protein levels for specific macromolecules occurred between 7 and 14 days after initiating hyperglycaemic conditions. Slot blot analysis showed 2–3-fold increases in mRNAs for collagen type I, fibronectin, versican and perlecan, whereas mRNA for decorin was increased by up to 20-fold. Levels of mRNAs for biglycan and syndecan were unaffected by hyperglycaemic culture. Reverse transcriptase PCR (RT–PCR) confirmed that decorin mRNA levels are greatly elevated and also showed increased transcription of the TGF-β1 gene in hyperglycaemic cultures. Western analysis and ELISA indicated accumulations of collagen types I and III, laminin and fibronectin in the cell layers and media of hyperglycaemic cultures with increasing time. Type IV collagen did not accumulate in either compartment of hyperglycaemic mesangial cell cultures. Collagen types I, III, and fibronectin did not accumulate in the cell layers of hyperglycaemic human dermal fibroblasts, indicating a cell-specific response in mesangial cultures. Decorin and versican, but not biglycan, were increased in the hyperglycaemic mesangial cell culture media. There were no apparent changes in core proteins for decorin and biglycan in fibroblast media. Transforming growth factor β1 (TGF-β1) in hyperglycaemic mesangial cell cultures increased 5-fold after 7 days, but decreased thereafter to only approx. 2-fold after 28 days. The changes in TGF-β1 mRNA, as detected by RT–PCR, and protein followed one another closely.

Glycated albumin stimulation of PKC-β activity is linked to increased collagen IV in mesangial cells

1999 ◽  
Vol 276 (5) ◽  
pp. F684-F690 ◽  
Author(s):  
Margo P. Cohen ◽  
Fuad N. Ziyadeh ◽  
Gregory T. Lautenslager ◽  
Jonathan A. Cohen ◽  
Clyde W. Shearman
Keyword(s):  
Collagen Type ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Glycated Albumin ◽  
Matrix Proteins ◽  
Collagen Type Iv ◽  
Type Iv ◽  
Pkc Β ◽  
Tgf Β1 ◽  
Stimulation Of

Albumin modified by Amadori-glucose adducts induces coordinate increases in the expression of extracellular matrix proteins, transforming growth factor (TGF)-β1, and the TGF-β type II receptor in glomerular mesangial cells. Because activation of protein kinase C (PKC) accompanies the increased mesangial cell expression of matrix proteins and TGF-β1 induced by high ambient glucose, we postulated that glycated albumin (GA) modulates PKC activity and that PKC participates in mediating the GA-induced stimulation of matrix production. To test this hypothesis, we examined the effects of PKC inhibitors on collagen type IV production by mouse or rat mesangial cells incubated with GA, and the influence of GA on PKC activity in these cells. Increased collagen type IV production evoked by GA in 5.5 and 25 mM glucose in mouse mesangial cells was prevented by both general (GF-109203X) and β-specific (LY-379196) PKC inhibitors. Total PKC activity, measured by phosphorylation of a PKC-specific substrate, increased with time after exposure of rat mesangial cells to GA compared with the nonglycated, glucose-free counterpart. GA caused an increase in PKC-β1 membrane-bound fraction and in total PKC activity in media containing physiological (5.5 mM) glucose concentrations in rat mesangial cells, confirming that the glucose-modified protein, and not a “hyperglycemic” milieu, was responsible. The findings indicate that Amadori-modified albumin stimulates mesangial cell PKC activity, and that activation of the PKC-β isoform is linked to the stimulation of collagen type IV production.

The Actions of C-Type Natriuretic Peptide on Human Mesangial Cell Apoptosis and P53 Expression

2000 ◽  
Vol 6 (S2) ◽  
pp. 624-625
Author(s):  
K. Seta ◽  
C. Wei
Keyword(s):  
Receptor Antagonist ◽  
Natriuretic Peptide ◽  
Cell Apoptosis ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Endocrine System ◽  
P53 Gene ◽  
Glomerular Mesangial Cells ◽  
P53 Expression ◽  
Human Mesangial Cell

C-type natriuretic peptide (CNP) of endothelial cell origin via NPR-B receptor mediates antimitogenic and vasodilatory actions. As a circulating endocrine system, CNP plays a fundamental role in cardiorenal regulation. However, the actions of CNP on renal mesangial cell apoptosis remain poorly defined. Apoptosis might plays an important role during development of renal glomerular mesangial cells pathophysiology. The mechanisms of apoptosis include p53-dependent pathway and p53-independent pathway.The hypothesis of this study is that CNP induces apoptosis through the process involving p53 gene in human glomerular mesangial cells via natriuretic peptide biological receptor. Therefore, the current study was designed to investigate the effects of CNP on apoptosis and p53 expression in human mesangial cell in the absence or presence of CNP biological receptor antagonist.Cultured human mesangial cells (Clontech Lab., San Diego, CA) was incubated for 24 hours in the absence or presence of CNP (10-7 M). These studies were repeated with HS 142-1 (HS, 10-5 M), a CNP biological receptor antagonist.

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