A new Cu(II)-based coordination polymer: treatment activity on the glomerulonephritis via inhibiting the mesangial cell proliferation

2021 ◽  
Author(s):  
Zheng Ye ◽  
Jingjing Xue ◽  
Jing Li ◽  
Xijing Wang ◽  
Fang Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Coordination Polymer ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Treatment Activity

scholarly journals Anti-angiogenic compound (TNP-470) inhibits mesangial cell proliferation in vitro and in vivo

1997 ◽  
Vol 51 (6) ◽  
pp. 1838-1846 ◽  
Author(s):  
Masashi Haraguchi ◽  
Mikio Okamura ◽  
Masayo Konishi ◽  
Yoshio Konishi ◽  
Nobuo Negoro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Proliferation In Vitro

Ramipril Inhibits in vitro Human Mesangial Cell Proliferation and Platelet-Derived Growth Factor Expression

1999 ◽  
Vol 7 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Giuseppe Grandaliano ◽  
Elena Ranieri ◽  
Raffaella Monno ◽  
Loreto Gesualdo ◽  
Francesco P. Schena
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Platelet Derived Growth Factor ◽  
Human Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Factor Expression ◽  
Growth Factor Expression

Suppression of Mesangial-Cell Proliferation by Trapidil in Glomerulonephritis Induced by Anti-Thymocyte Serum in Rats

1995 ◽  
Vol 23 (6) ◽  
pp. 458-466 ◽  
Author(s):  
M S Razzaque ◽  
M Cheng ◽  
T Taguchi
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Single Dose ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Platelet Derived Growth Factor ◽  
Group Iii ◽  
Group I ◽  
Mesangial Cell Proliferation ◽  
Group Ii

Trapadil (Mochida Pharmaceuticals, Japan), an antiplatelet drug, suppresses the growth of several cell types and is thought to antagonize platelet-derived growth factor. The effects of trapidil on mesangial-cell proliferation in glomerulonephritis induced by anti-thymocyte serum in Wistar rats were investigated. Control rats were treated with phosphate-buffered saline (group I); group II rats were injected with a single dose of anti-thymocyte serum (8 ml/kg body weight), and group III rats were treated with both a single dose of anti-thymocyte serum (8 ml/kg body weight) and with trapidil (5 mg/kg body weight/day). Three rats in each group were killed on day 3, and the other three on day 10. Control rats showed no significant histological changes on day 3 or day 10. In group II, on day 3, there was a marked decrease in glomerular cell numbers, with mesangiolysis. Histologically severe mesangial-cell proliferation with expansion of mesangial areas was noted on day 10. None of the rats in group III showed mesangial alterations, histologically, indicating that mesangial-cell proliferation was suppressed by trapidil. This suppression may result from antagonism of the binding of platelet derived growth factor to the specific surface receptors in the mesangial cells. Trapidil may have clinical value in the treatment of mesangial-cell proliferative glomerular diseases.

scholarly journals Effect of bradykinin on renal mesangial cell proliferation and extracellular matrix secretion

2014 ◽  
Vol 13 (1) ◽  
pp. 490-498 ◽  
Author(s):  
C.Y. Liu ◽  
L.L. Zhou ◽  
Q. Cheng ◽  
S.N. Jiang ◽  
J. Sheng ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Extracellular Matrix Secretion

scholarly journals 15-Deoxy-Δ12,14-prostaglandin J2 regulates mesangial cell proliferation and death

2002 ◽  
Vol 61 (4) ◽  
pp. 1293-1302 ◽  
Author(s):  
Brad H. Rovin ◽  
William A. Wilmer ◽  
Ling Lu ◽  
Andrea I. Doseff ◽  
Cynthia Dixon ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Prostaglandin J2

Effect of interleukin-6 receptor blockage on renal injury in apolipoprotein E-deficient mice

2009 ◽  
Vol 297 (3) ◽  
pp. F679-F684 ◽  
Author(s):  
Mari Tomiyama-Hanayama ◽  
Hiromi Rakugi ◽  
Masaharu Kohara ◽  
Toru Mima ◽  
Yasuo Adachi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Apolipoprotein E ◽  
Interleukin 6 ◽  
Renal Injury ◽  
Mesangial Cell ◽  
Organ Damage ◽  
Glomerular Injury ◽  
Mesangial Cell Proliferation ◽  
Matrix Expansion ◽  
Interleukin 6 Receptor

Hyperlipidemia has been demonstrated to be associated with renal disease, yet the mechanism of renal injury is still poorly understood. Inflammation that occurs with the hyperlipidemia has been considered to play an important role in development of glomerular injury. In the present study, we investigated the role of interleukin-6 (IL-6), a key inflammatory molecule, on renal injury in apolipoprotein E-deficient (ApoE−/−) mice with severe hypercholesterolemia. The 6-wk-old mice were fed a high-fat diet and administered weekly rat anti-IL-6 receptor monoclonal antibody (MR16-1), control rat IgG, or saline for a total of 4 wk. We examined histopathological changes in the kidney and urinary excretion of protein and albumin. Saline- and IgG-treated mice showed remarkable proteinuria at 10 wk of age, whereas MR16-1-treated mice exhibited significantly lower levels. Renal histopathology of saline- and IgG-treated mice revealed striking lipid deposits and foam cells in the glomerular tuft, juxtaglomerular area, and arteriolar wall along with range of mesangial cell proliferation and matrix expansion. Notably, the severity of lipid deposits and mesangial cell proliferation were significantly reduced in MR16-1-treated mice. Immunohistochemistry demonstrated that mesangial IL-6 expression was dramatically reduced in MR16-1-treated mice compared with IgG-treated mice. Blocking the IL-6 receptor prevented progression of proteinuria and renal lipid deposit, as well as the mesangial cell proliferation associated with severe hyperlipoproteinemia. These results clearly demonstrate that IL-6 plays an essential role in the pathogenesis of hyperlipidemia-induced glomerular injury in ApoE−/− mice and suggests the usefulness of anti-IL-6 receptor antibody in treatments for hyperlipidemia-induced organ damage.

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