Modulation by Angiotensin II of Endothelial Cell Control of DNA Synthesis in Human Mesangial Cells

Nephron ◽  
1997 ◽  
Vol 75 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Marie Essig ◽  
Jean-Claude Dussaule ◽  
Sophie Vandermeersch ◽  
Christos Chatziantoniou ◽  
Raymond Ardaillou
Keyword(s):  
Endothelial Cell ◽  
Angiotensin Ii ◽  
Dna Synthesis ◽  
Mesangial Cells ◽  
Cell Control ◽  
Human Mesangial Cells

Soluble uric acid increases intracellular calcium through an angiotensin II-dependent mechanism in immortalized human mesangial cells

2010 ◽  
Vol 235 (7) ◽  
pp. 825-832 ◽  
Author(s):  
Guilherme Albertoni ◽  
Edgar Maquigussa ◽  
Edson Pessoa ◽  
Jose Augusto Barreto ◽  
Fernanda Borges ◽  
...  
Keyword(s):  
Uric Acid ◽  
Angiotensin Ii ◽  
Intracellular Calcium ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Dependent Mechanism

c-Jun NH2-terminal kinase mediation of angiotensin II-induced proliferation of human mesangial cells

2005 ◽  
Vol 288 (6) ◽  
pp. F1118-F1124 ◽  
Author(s):  
Aihua Zhang ◽  
Guixia Ding ◽  
Songming Huang ◽  
Yuanjun Wu ◽  
Xiaoqing Pan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Angiotensin Ii ◽  
Map Kinases ◽  
Mesangial Cells ◽  
Cell Number ◽  
Renal Diseases ◽  
Steady Increase ◽  
Dependent Manner ◽  
Ang Ii ◽  
Human Mesangial Cells

Angiotensin II (ANG II) has been shown to activate c-Jun NH2-terminal kinase (JNK) in cultured mesangial cells, but the functional implication of this phenomenon remains to be determined, largely due to the lack of an effective approach to block JNK. Therefore, the present study was carried out to examine whether JNK is involved in ANG II-induced cell proliferation in cultured human mesangial cells (HMCs) with the use of a newly developed JNK-selective blocker, SP-600125. Within minutes, treatment with 100 nM ANG II activated all three members of MAP kinase family, including extracellular signal-regulated protein kinase (Erk) 1/2, JNK, and p38 in cultured HMCs, as assessed by immunoblotting detection of phosphorylation of MAP kinases. ANG II-dependent activation of JNK was further confirmed by detection of increased phosphorylation and transcription activity of c-Jun after the ANG II treatment. SP-600125 ranging from 5 to 10 μM almost completely abolished the activation of JNK by ANG II without affecting the activities of Erk1/2 and p38. After treatment with 100 ng ANG II, there was a steady increase in [3H]thymidine incorporation that was blocked by SP-60025 in a dose- and time-dependent manner. Similarly, SP-600125 dose dependently reduced the ANG II-induced increase in cell number. The antiproliferative effect of SP-60025 was further determined by cell-cycle analysis with flow cytometry. Twenty-four hours after ANG II treatment, 50% of the quiescent HMCs (G0/G1) progressed into the S phase, and the cell cycle progression was almost completely prevented in the presence of SP-60025. Our data suggest that JNK mediates the proliferative effect of ANG II in cultured HMCs and thus represents a novel therapeutic target for treatment of chronic renal diseases.

Endothelin modulates angiotensin II-induced mitogenesis of human mesangial cells

1993 ◽  
Vol 264 (6) ◽  
pp. F937-F942 ◽  
Author(s):  
G. L. Bakris ◽  
R. N. Re
Keyword(s):  
Angiotensin Ii ◽  
Mesangial Cell ◽  
Thymidine Incorporation ◽  
Mesangial Cells ◽  
Culture Conditions ◽  
Ang Ii ◽  
Mitogenic Effect ◽  
Mitogenic Response ◽  
Human Mesangial Cells ◽  
Cell Counts

Angiotensin II (ANG II) elicits either a hypertrophic or hyperplastic response depending on culture conditions. Human mesangial cell (HMC)-generated endothelin (ET) plays a role in mediating the hyperplastic effects of arginine vasopressin. The interaction between ANG II and ET is not described in HMC. The present study evaluates the possible effect of ANG II on HMC production of ET, its relationship to mitogenesis, and the effect of insulin. ANG II (10(-8) M) increased [3H]thymidine incorporation in proliferative HMC at 48 h (13 +/- 1 vs. 24 +/- 1 x 10(3) counts.min-1.well-1, for control vs. ANG II; P < 0.05). Cell counts showed parallel increases [12 +/- 1 (control) vs. 18 +/- 1 x 10(3) counts/well; P < 0.05]. This mitogenic effect was attenuated by a monoclonal antibody to ET-1 or the ANG II-receptor antagonist, DuP 753. Insulin potentiated the mitogenic response of ANG II through increases in HMC ET production (69 +/- 7 vs. 189 +/- 13 pg/ml, for insulin alone vs. insulin+ANG II; P < 0.05). This study supports the concept that ANG II may act as a mitogen under certain culture conditions and its effect is, in part, mediated through ET.

Sign in / Sign up

Export Citation Format

Share Document