TGF-β1 inducible genes in coronary smooth muscle cells

2004 ◽  
Vol 2004 (Fall) ◽  
Author(s):  
Stefan Lorkowski ◽  
Katrin Stolle ◽  
Michael Schnoor ◽  
J�rgen Rauterberg ◽  
Paul Cullen
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Coronary Smooth Muscle ◽  
Inducible Genes ◽  
Tgf Β1

IGFBP-3 activates TGF-β receptors and directly inhibits growth in human intestinal smooth muscle cells

2004 ◽  
Vol 287 (4) ◽  
pp. G795-G802 ◽  
Author(s):  
John F. Kuemmerle ◽  
Karnam S. Murthy ◽  
Jennifer G. Bowers
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Nuclear Translocation ◽  
Thymidine Incorporation ◽  
Muscle Cells ◽  
Serine Phosphorylation ◽  
Intestinal Smooth Muscle ◽  
Igf I ◽  
Tgf Β1 ◽  
Igfbp 3

We have shown that human intestinal smooth muscle cells produce IGF-I and IGF binding protein-3 (IGFBP-3). Endogenous IGF-I acts in autocrine fashion to stimulate growth of these cells. IGFBP-3 inhibits the binding of IGF-I to its receptor and thereby inhibits IGF-I-stimulated growth. In several carcinoma cell lines and some normal cells, IGFBP-3 regulates growth independently of IGF-I. Two mechanisms for this effect have been identified: IGFBP-3 can directly activate transforming growth factor-β (TGF-β) receptors or it can undergo direct nuclear translocation. The aim of the present study was to determine whether IGFBP-3 acts independently of IGF-I and to characterize the mechanisms mediating this effect in human intestinal smooth muscle cells. The direct effects of IGFBP-3 were determined in the presence of an IGF-I receptor antagonist to eliminate its IGF-I-dependent effects. Affinity labeling of TGF-β receptors (TGF-βRI, TGF-βRII, and TGF-βRV) with 125I-labeled TGF-β1 showed that IGFBP-3 displaced binding to TGF-βRII and TGF-βRV in a concentration-dependent fashion. IGFBP-3 stimulated TGF-βRII-dependent serine phosphorylation (activation) of both TGF-βRI and of its primary substrate, Smad2(Ser465/467). IGFBP-3 also caused IGF-I-independent inhibition of basal [3H]thymidine incorporation. The effects of IGFBP-3 on Smad2 phosphorylation and on smooth muscle cell proliferation were independent of TGF-β1 and were abolished by transfection of Smad2 siRNA. Immunoneutralization of IGFBP-3 increased basal [3H]thymidine incorporation, implying that endogenous IGFBP-3 inhibits proliferation. We conclude that endogenous IGFBP-3 directly inhibits proliferation of human intestinal smooth muscle cells by activation of TGF-βRI and Smad2, an effect that is independent of its effect on IGF-I-stimulated growth.

Ethanol Modulates Cyclic GMP Metabolism in Cultured Coronary Smooth Muscle Cells

Angiology ◽  
1993 ◽  
Vol 44 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Yukio Kishi ◽  
Toshiyuki Oniki ◽  
Takashi Ashikaga ◽  
Fujio Numano
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cyclic Gmp ◽  
Muscle Cells ◽  
Coronary Smooth Muscle

scholarly journals Evidence for Oxidative Activation of c-Myc–Dependent Nuclear Signaling in Human Coronary Smooth Muscle Cells and in Early Lesions of Watanabe Heritable Hyperlipidemic Rabbits

Circulation ◽  
2000 ◽  
Vol 102 (17) ◽  
pp. 2111-2117 ◽  
Author(s):  
Filomena de Nigris ◽  
Tammam Youssef ◽  
SilviaAnna Ciafré ◽  
Flavia Franconi ◽  
Vittorio Anania ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Coronary Smooth Muscle ◽  
Nuclear Signaling ◽  
Early Lesions ◽  
Oxidative Activation

scholarly journals Maternal nutrient restriction during pregnancy impairs an endothelium-derived hyperpolarizing factor-like pathway in sheep fetal coronary arteries

2014 ◽  
Vol 307 (2) ◽  
pp. H134-H142 ◽  
Author(s):  
Praveen Shukla ◽  
Srinivas Ghatta ◽  
Nidhi Dubey ◽  
Caleb O. Lemley ◽  
Mary Lynn Johnson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
National Research Council ◽  
Muscle Cells ◽  
Nutrient Restriction ◽  
Epoxyeicosatrienoic Acid ◽  
Coronary Smooth Muscle ◽  
Maternal Undernutrition ◽  
Current Activation

The mechanisms underlying developmental programming are poorly understood but may be associated with adaptations by the fetus in response to changes in the maternal environment during pregnancy. We hypothesized that maternal nutrient restriction during pregnancy alters vasodilator responses in fetal coronary arteries. Pregnant ewes were fed a control [100% U.S. National Research Council (NRC)] or nutrient-restricted (60% NRC) diet from days 50 to 130 of gestation (term = 145 days); fetal tissues were collected at day 130. In coronary arteries isolated from control fetal lambs, relaxation to bradykinin was unaffected by nitro-l-arginine (NLA). Iberiotoxin or contraction with KCl abolished the NLA-resistant response to bradykinin. In fetal coronary arteries from nutrient-restricted ewes, relaxation to bradykinin was fully suppressed by NLA. Large-conductance, calcium-activated potassium channel (BKCa) currents did not differ in coronary smooth muscle cells from control and nutrient-restricted animals. The BKCa openers, BMS 191011 and NS1619, and 14,15-epoxyeicosatrienoic acid [a putative endothelium-derived hyperpolarizing factor (EDHF)] each caused fetal coronary artery relaxation and BKCa current activation that was unaffected by maternal nutrient restriction. Expression of BKCa-channel subunits did not differ in fetal coronary arteries from control or undernourished ewes. The results indicate that maternal undernutrition during pregnancy results in loss of the EDHF-like pathway in fetal coronary arteries in response to bradykinin, an effect that cannot be explained by a decreased number or activity of BKCa channels or by decreased sensitivity to mediators that activate BKCa channels in vascular smooth muscle cells. Under these conditions, bradykinin-induced relaxation is completely dependent on nitric oxide, which may represent an adaptive response to compensate for the absence of the EDHF-like pathway.

scholarly journals Carvedilol Inhibits Pressure-Induced Increase in Oxidative Stress in Coronary Smooth Muscle Cells.

2002 ◽  
Vol 25 (3) ◽  
pp. 419-425 ◽  
Author(s):  
Kenichi YASUNARI ◽  
Kensaku MAEDA ◽  
Munehiro NAKAMURA ◽  
Junichi YOSHIKAWA
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Coronary Smooth Muscle
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