scholarly journals COX-2/mPGES-1/PGE2 cascade activation mediates uric acid-induced mesangial cell proliferation

Oncotarget ◽  
2016 ◽  
Vol 8 (6) ◽  
pp. 10185-10198 ◽  
Author(s):  
Shuzhen Li ◽  
Zhenzhen Sun ◽  
Yue Zhang ◽  
Yuan Ruan ◽  
Qiuxia Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Uric Acid ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Cox 2

scholarly journals mPGES-1-Derived PGE2 Contributes to Indoxyl Sulfate-Induced Mesangial Cell Proliferation

2017 ◽  
Vol 43 (1) ◽  
pp. 271-281
Author(s):  
Shuzhen Li ◽  
Zhenzhen Sun ◽  
Guixia Ding ◽  
Wei Gong ◽  
Jing Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Cell Number ◽  
Pathological Process ◽  
Indoxyl Sulfate ◽  
Prostaglandin E ◽  
Mrna Levels ◽  
Mesangial Cell Proliferation ◽  
Cox 2

Background/Aims: We previously reported that indoxyl sulfate (IS) could cause mesangial cell (MC) proliferation via a cyclooxygenase (COX)-2-dependent mechanism. However, the specific prostaglandin contributing to COX-2 effect on IS-induced MC proliferation remained unknown. Thus, the present study was undertaken to examine the role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived Prostaglandin E2 (PGE2) in IS-induced MC proliferation. Methods: IS was administered to the MCs with or without mPGES-1 siRNA pretreatment to induce the MC proliferation which was determined by cell cycle analysis, DNA synthesis, and the expressions of cyclins. In another experimental setting, PGE2 was applied to the MCs to examine its direct effect on MC proliferation, as well as the regulation of prostaglandin E receptors (EPs) by qRT-PCR. Results: With the administration of IS, mPGES-1(not mPGES-2 and cytosolic PGES) was significantly upregulated at both protein and mRNA levels in line with a promoted MC proliferation. Interestingly, silencing mPGES-1 reduced cell number in S and G2 phases and blocked the upregulation of cyclin A2 and cyclin D1 in parallel with blunted PGE2 release after IS treatment, indicating that mPGES-1-derived PGE2 could contribute to MC proliferation. Furthermore, we confirmed that exogenous PGE2 could directly trigger the proliferative response in MCs. Lastly, we observed a selective upregulation of EP2 after PGE2 treatment and enhanced phosphorylation of NF-κB following IS administration in MCs, suggesting the potential involvements of EP2 and NF-κB in this pathological process. Conclusion: mPGES-1-derived PGE2 contributed to IS-induced mesangial cell proliferation.

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

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
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