Antibodies against a putative heparin receptor slow cell proliferation and decrease MAPK activation in vascular smooth muscle cells

2001 ◽  
Vol 187 (3) ◽  
pp. 283-293 ◽  
Author(s):  
Joyce M. Savage ◽  
Albert C. Gilotti ◽  
Catherine A. Granzow ◽  
Felix Molina ◽  
Linda J. Lowe-Krentz
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mapk Activation

scholarly journals Troglitazone and pioglitazone attenuate agonist-dependent Ca2+ mobilization and cell proliferation in vascular smooth muscle cells

1999 ◽  
Vol 128 (3) ◽  
pp. 673-683 ◽  
Author(s):  
Michiko Asano ◽  
Toshiaki Nakajima ◽  
Kuniaki Iwasawa ◽  
Toshihiro Morita ◽  
Fumitaka Nakamura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

Leptin increases endothelin type A receptor levels in vascular smooth muscle cells

2008 ◽  
Vol 294 (3) ◽  
pp. E481-E487 ◽  
Author(s):  
Chi-Chang Juan ◽  
Tung-Yueh Chuang ◽  
Chih-Chen Lien ◽  
Yen-Jie Lin ◽  
Seng-Wong Huang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Type A ◽  
Northern Blotting ◽  
Dose Dependent

Leptin, one of the adipocyte-secreted peptides, is involved in the control of appetite and body weight. Several studies have demonstrated that plasma leptin levels are elevated in obese subjects and are positively correlated with body weight. The arterial endothelin (ET) system plays an important role in the regulation of vascular tone, and ET-1 overexpression may be involved in the pathogenesis of the hypertension associated with insulin resistance. This study was performed to explore the regulatory effects of leptin on ET receptor expression and ET binding in A10 vascular smooth muscle cells (VSMCs) by use of Northern blotting, immunoblotting, and a 125I-labeled ET-1 binding assay. The effect of leptin on ET receptor-mediated cell proliferation was also tested. The results showed that leptin caused a significant increase in [125I]-ET-1 binding, which was time- and dose-dependent. Immunoblotting showed that expression of the ET type A receptor (ETAR) in leptin (10−7 M)-treated cells was increased by up to 2.3-fold compared with controls. Levels of ETAR mRNA measured by Northern blotting were also increased by up to 2.2-fold in leptin (10−7 M)-treated cells. Pretreatment with an ERK inhibitor, PD-98059 (2.5 × 10−5 M), blocked the leptin-induced increase in 125I-ET-1 binding. Finally, ET-1 (10−7 M)-stimulated cell proliferation was enhanced by leptin (10−7 M) pretreatment, with a maximal increase of twofold compared with controls. In conclusion, leptin increases ETAR expression in VSMCs in a time- and dose-dependent manner. This effect is ERK dependent and is associated with increased ET-1-stimulated cell proliferation. These findings provide support for roles for leptin and the ET system in the pathogenesis of obesity-associated hypertension.

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