American Gastroenterological Association Workshop on Smooth-muscle Physiology

1978 ◽  
Vol 23 (10) ◽  
pp. 948-951
Author(s):  
James Christensen ◽  
Sidney Cohen

One of the earliest studies on the physiology of smooth muscle was that reported by Engelmann over 100 years ago. In setting the stage for this discussion on new developments in smooth muscle physiology, Professor Bozler recalled Engelmann’s description of the ureter as a ‘giant hollow muscle fibre’. Recent work on the passive electrical properties of smooth muscle has shown that Engelmann’s concept of the syncytial behaviour of smooth muscle is true for a great many smooth muscles - perhaps for all vertebrate smooth muscles. When smooth muscle cells come into contact they interact with each other so as to form a tissue. In this sense, a community of smooth muscle cells is analogous with the liver, epithelial tissues and the heart. One can contrast this ‘collective’ behaviour of smooth muscle cells with the separate identity maintained by most nerve cells and skeletal muscle fibres.


2017 ◽  
Vol 68 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Akira Takai ◽  
Masumi Eto ◽  
Katsuya Hirano ◽  
Kosuke Takeya ◽  
Toshiyuki Wakimoto ◽  
...  

2008 ◽  
Vol 294 (1) ◽  
pp. L57-L68 ◽  
Author(s):  
Pawan Sharma ◽  
Thai Tran ◽  
Gerald L. Stelmack ◽  
Karol McNeill ◽  
Reinoud Gosens ◽  
...  

Airway smooth muscle (ASM) cells may contribute to asthma pathogenesis through their capacity to switch between a synthetic/proliferative and a contractile phenotype. The multimeric dystrophin-glycoprotein complex (DGC) spans the sarcolemma, linking the actin cytoskeleton and extracellular matrix. The DGC is expressed in smooth muscle tissue, but its functional role is not fully established. We tested whether contractile phenotype maturation of human ASM is associated with accumulation of DGC proteins. We compared subconfluent, serum-fed cultures and confluent cultures subjected to serum deprivation, which express a contractile phenotype. Western blotting confirmed that β-dystroglycan, β-, δ-, and ε-sarcoglycan, and dystrophin abundance increased six- to eightfold in association with smooth muscle myosin heavy chain (smMHC) and calponin accumulation during 4-day serum deprivation. Immunocytochemistry showed that the accumulation of DGC subunits was specifically localized to a subset of cells that exhibit robust staining for smMHC. Laminin competing peptide (YIGSR, 1 μM) and phosphatidylinositol 3-kinase (PI3K) inhibitors (20 μM LY-294002 or 100 nM wortmannin) abrogated the accumulation of smMHC, calponin, and DGC proteins. These studies demonstrate that the accumulation of DGC is an integral feature for phenotype maturation of human ASM cells. This provides a strong rationale for future studies investigating the role of the DGC in ASM smooth muscle physiology in health and disease.


Asthma ◽  
2014 ◽  
pp. 321-333
Author(s):  
Erick Forno ◽  
Louis-Philippe Boulet ◽  
Juan C. Celedón

The current epidemiologic and experimental evidence for a causal association between obesity and asthma is reviewed in this chapter. Putative mechanisms underlying the association between obesity and asthma, including genetics, changes in lung mechanics and airway smooth muscle physiology, hormonal differences, and detrimental effects of comorbidities and the systemic proinflammatory state of obesity are also discussed. These proposed causal pathways are largely speculative or insufficiently studied. Whereas obesity seems to be closely interrelated with the pathogenesis of asthma in some subjects who have the true “obese asthmatic phenotype,” obesity may simply coexist with asthma in others. Proper identification of subjects with true “obese asthma” may be key to dissecting any causal mechanism. Weight loss is beneficial and should be recommended for obese adults with asthma.


Sign in / Sign up

Export Citation Format

Share Document