Vasodilator Agents Modulate Rat Glomerular Mesangial Cell Growth and Collagen Synthesis

Nephron ◽  
1995 ◽  
Vol 70 (1) ◽  
pp. 91-99 ◽  
Author(s):  
Tun-Jun Tsai ◽  
Rong-Hwa Lin ◽  
Chih-Cheng Chang ◽  
Yung-Ming Chen ◽  
Chau-Fong Chen ◽  
...  
2001 ◽  
Vol 280 (4) ◽  
pp. F667-F674 ◽  
Author(s):  
Chhinder P. Sodhi ◽  
Sarojini A. Phadke ◽  
Daniel Batlle ◽  
Atul Sahai

The effect of hypoxia on the proliferation and collagen synthesis of cultured rat mesangial cells was examined under normal-glucose (NG, 5 mM) and high-glucose (HG, 25 mM)-media conditions. In addition, a role for osteopontin (OPN) in mediating these processes was assessed. Quiescent cultures were exposed to hypoxia (3% O2) and normoxia (18% O2) in a serum-free medium with NG or HG, and cell proliferation, collagen synthesis, and OPN expression were assessed. Cells exposed to hypoxia in NG medium resulted in significant increases in [3H]thymidine incorporation, cell number, and [3H]proline incorporation, respectively. HG incubations also produced significant stimulation of these parameters under normoxic conditions, which were markedly enhanced in cells exposed to hypoxia in HG medium. In addition, hypoxia and HG stimulated the mRNA levels of type IV collagen, and the combination of hypoxia and HG resulted in additive increases in type IV collagen expression. Hypoxia and HG also stimulated OPN mRNA and protein levels in an additive fashion. A neutralizing antibody to OPN or its β3-integrin receptor significantly blocked the effect of hypoxia and HG on proliferation and collagen synthesis. In conclusion, these results demonstrate for the first time that hypoxia in HG medium produces exaggerated mesangial cell growth and type IV collagen synthesis. In addition, OPN appears to play a role in mediating the accelerated mesangial cell growth and collagen synthesis found in a hyperglycemic and hypoxic environment.


Hypertension ◽  
1998 ◽  
Vol 32 (5) ◽  
pp. 945-952 ◽  
Author(s):  
Peter Rene Mertens ◽  
Volker Espenkott ◽  
Birgit Venjakob ◽  
Bernhard Heintz ◽  
Stefan Handt ◽  
...  

1991 ◽  
Vol 32 (1-2) ◽  
pp. 109-111 ◽  
Author(s):  
H. H. Radeke ◽  
B. Schwinzer ◽  
J. Ohe ◽  
C. Bovenkerk ◽  
K. Resch

2010 ◽  
Vol 333 (3) ◽  
pp. 808-815 ◽  
Author(s):  
Raghvendra K. Dubey ◽  
Marinella Rosselli ◽  
Delbert G. Gillespie ◽  
Zaichuan Mi ◽  
Edwin K. Jackson

2021 ◽  
Vol 22 (14) ◽  
pp. 7589
Author(s):  
Anberitha T. Matthews ◽  
Hitesh Soni ◽  
Katherine E. Robinson-Freeman ◽  
Theresa A. John ◽  
Randal K. Buddington ◽  
...  

Doxorubicin (DOX), a category D pregnancy drug, is a chemotherapeutic agent that has been shown in animal studies to induce fetal toxicity, including renal abnormalities. Upregulation of the transient receptor potential cation (TRPC) 6 channel is involved in DOX-induced podocyte apoptosis. We have previously reported that TRPC6-mediated Ca2+ signaling promotes neonatal glomerular mesangial cell (GMC) death. However, it is unknown whether DOX alters mesangial TRPC expression or viability in the fetus. In this study, cell growth was tracked in control and DOX-treated primary GMCs derived from fetal pigs. Live-cell imaging demonstrated that exposure to DOX inhibited the proliferation of fetal pig GMCs and induced cell death. DOX did not alter the TRPC3 expression levels. By contrast, TRPC6 protein expression in the cells was markedly reduced by DOX. DOX treatment also attenuated the TRPC6-mediated intracellular Ca2+ elevation. DOX stimulated mitochondrial reactive oxygen species (mtROS) generation and mitophagy by the GMCs. The DOX-induced mtROS generation and apoptosis were reversed by the mitochondria-targeted antioxidant mitoquinone. These data suggest that DOX-induced fetal pig GMC apoptosis is independent of TRPC6 channel upregulation but requires mtROS production. The mtROS-dependent GMC death may contribute to DOX-induced fetal nephrotoxicity when administered prenatally.


2021 ◽  
pp. 110072
Author(s):  
Falguni Das ◽  
Amit Bera ◽  
Nandini Ghosh-Choudhury ◽  
Kavitha Sataranatarajan ◽  
Amrita Kamat ◽  
...  

2009 ◽  
Vol 219 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Victoriya A. Rufanova ◽  
Anna Alexanian ◽  
Tetsuro Wakatsuki ◽  
Adam Lerner ◽  
Andrey Sorokin

2016 ◽  
Vol 198 (3) ◽  
pp. 1104-1118 ◽  
Author(s):  
Ganqian Zhu ◽  
Wen Qiu ◽  
Yongting Li ◽  
Chenhui Zhao ◽  
Fengxia He ◽  
...  

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