Dissociation of K+-induced tension and cellular Ca2+ retention in vascular and intestinal smooth muscle in normoxia and hypoxia

1982 ◽  
Vol 394 (2) ◽  
pp. 118-123 ◽  
Author(s):  
H. Karaki ◽  
T. Suzuki ◽  
H. Ozaki ◽  
N. Urakawa ◽  
Y. Ishida
Keyword(s):  
Smooth Muscle ◽  
Intestinal Smooth Muscle

Role of stat6 in hypercontractility of murine small intestinal smooth muscle induced by nematode infection

2001 ◽  
Vol 120 (5) ◽  
pp. A534-A534
Author(s):  
A ZHAO ◽  
D MULLOY ◽  
J URBANJR ◽  
W GAUSE ◽  
T SHEADONOHUE
Keyword(s):  
Smooth Muscle ◽  
Nematode Infection ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

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.

Hymenolepis diminuta:Mucosal Mastocytosis and Intestinal Smooth Muscle Hypertrophy Occur in Tapeworm-Infected Rats

1998 ◽  
Vol 89 (1) ◽  
pp. 92-102 ◽  
Author(s):  
Michael B. Dwinell ◽  
Ruth M. Wise ◽  
Paul Bass ◽  
John A. Oaks
Keyword(s):  
Smooth Muscle ◽  
Muscle Hypertrophy ◽  
Intestinal Smooth Muscle

Histamine-operated calcium channels in intestinal smooth muscle of the guinea-pig

1987 ◽  
Vol 135 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Nicole Morel ◽  
Jean-Paul Hardy ◽  
Théophile Godfraind
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Calcium Channels ◽  
Intestinal Smooth Muscle

The effects of acetylcholine and atropine on the 22Na+ permeability of intestinal smooth muscle vesicles

1978 ◽  
Vol 56 (6) ◽  
pp. 921-925
Author(s):  
L. Spero
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Membrane Vesicles ◽  
Intestinal Smooth Muscle ◽  
Erythrocyte Ghosts ◽  
Muscarinic Agonists ◽  
Plasma Membrane Vesicles ◽  
Muscle Plasma Membrane ◽  
Whole Muscle ◽  
Kinetics Of

A technique is described which has enabled us to measure changes in 22Na+ efflux from smooth muscle plasma membrane vesicles. The resting 22Na+ efflux from these sealed vesicles showed a concentration-dependent increase in response to acetylcholine and other muscarinic agonists, in similar concentrations to those which increased 42K+ efflux in whole muscle. The kinetics of this efflux were complex and could not be described by less than three exponential processes. The response to agonists has, therefore, been characterized by measurement of the half-life of 22Na+ efflux (t1/2). The acetylcholine effect was inhibited by atropine, but unlike the situation in the whole muscle, this inhibition was noncompetitive. Tubocuraine (a nicotinic antagonist) had no effect on this acetylcholine response. Atropine has no effect by itself on the resting 22Na+ efflux, neither did tetrodotoxin or ouabain. 22Na+ efflux from erythrocyte ghosts and liposomes, prepared from lipid extracts of the smooth muscle plasma membrane, was not modified by acetylcholine or atropine.

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