Increased Mechanical Strain In Vivo Using Continuous Positive Airway Pressure Reduces Murine Airway Reactivity In Vivo And Regulates Expression Of Smooth Muscle Myosin Heavy Chain

2012 ◽  
Author(s):  
Zhidong C. Xue ◽  
Leena Desai ◽  
Wenwu Zhang ◽  
Susan J. Gunst ◽  
Robert S. Tepper
Keyword(s):  
Smooth Muscle ◽  
Continuous Positive Airway Pressure ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Mechanical Strain ◽  
Airway Reactivity ◽  
Muscle Myosin

scholarly journals Chronic continuous positive airway pressure (CPAP) reduces airway reactivity in vivo in an allergen-induced rabbit model of asthma

2011 ◽  
Vol 111 (2) ◽  
pp. 353-357 ◽  
Author(s):  
Z. Xue ◽  
Y. Yu ◽  
H. Gao ◽  
S. J. Gunst ◽  
R. S. Tepper
Keyword(s):  
Continuous Positive Airway Pressure ◽  
Airway Inflammation ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Mechanical Strain ◽  
Rabbit Model ◽  
Therapeutic Benefit ◽  
Airway Responsiveness ◽  
Airway Reactivity

Previous studies have demonstrated that chronic mechanical strain produced by continuous positive airway pressure (CPAP) reduces in vivo airway reactivity in rabbits and ferrets. For CPAP to potentially have a therapeutic benefit for asthmatic subjects, the reduction in airway responsiveness would need to persist for 12–24 h after its discontinuation, require application for only part of the day, and be effective in the presence of atopic airway inflammation. In the present study, airway responsiveness to acetylcholine or methacholine was measured during mechanical ventilation following three different protocols in which active, nonanesthetized, tracheotomized rabbits were treated with High vs. Low CPAP (6 vs. 0 cmH2O). 1) High CPAP was applied continuously for 4 days followed by 1 day of Low CPAP; 2) High CPAP was applied at night and Low CPAP during the daytime for 4 days, and 3) High CPAP was applied for 4 days in animals following ovalbumin (Ova) sensitization and challenge. For all three protocols, treatment with High CPAP resulted in significantly reduced airway responsiveness compared with treatment with Low CPAP. Cumulatively, our in vivo results in rabbits suggest that high CPAP, even when applied only at night, produces a persistent reduction of airway responsiveness. In addition, CPAP reduces airway responsiveness even in the presence of atopic airway inflammation.

Respiratory system responsiveness in rabbits in vivo is reduced by prolonged continuous positive airway pressure

2005 ◽  
Vol 99 (2) ◽  
pp. 677-682 ◽  
Author(s):  
Z. Xue ◽  
L. Zhang ◽  
R. Ramchandani ◽  
Y. Liu ◽  
V. B. Antony ◽  
...  
Keyword(s):  
Continuous Positive Airway Pressure ◽  
Respiratory System ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Mechanical Strain ◽  
Airway Reactivity ◽  
Airway Function ◽  
System Responsiveness

Active, nonanesthetized, tracheotomized rabbits were subjected to continuous positive airway pressure (CPAP) for 4 days to determine the effects of chronic mechanical strain on lung and airway function. Rabbits were maintained for 4 days at a CPAP of 6 cmH2O (high CPAP), at a CPAP of 0 cmH2O (low CPAP), or without tracheostomy (no CPAP). After treatment with CPAP, changes in respiratory resistance in response to increasing concentrations of inhaled ACh were measured during mechanical ventilation to evaluate respiratory system responsiveness in vivo. Intraparenchymal bronchial segments were isolated from the lungs of all animals to evaluate airway smooth muscle responsiveness and bronchial compliance in vitro. Rabbits maintained for 4 days at high CPAP demonstrated significantly lower responsiveness to ACh compared with rabbits that were maintained at low CPAP or with no CPAP. Airways isolated from the lungs of animals subjected to the chronic application of high CPAP were also less responsive to ACh in vitro than the airways isolated from animals subjected to low CPAP or no CPAP. The persistence of the decreased responsiveness in the excised airway tissues suggests that the decreased respiratory system responsiveness observed in vivo results primarily from direct effects on the airways. The results demonstrate that the application of prolonged mechanical strain in vivo can reduce airway reactivity.

Expression and function of COOH-terminal myosin heavy chain isoforms in mouse smooth muscle

2007 ◽  
Vol 293 (1) ◽  
pp. C238-C245 ◽  
Author(s):  
Anne F. Martin ◽  
Sunita Bhatti ◽  
Gail J. Pyne-Geithman ◽  
Mariam Farjah ◽  
Vlasios Manaves ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Immunoblot Analysis ◽  
Myosin Heavy Chain Isoforms ◽  
Smooth Muscle Myosin ◽  
Tail Region ◽  
Protein Ratio ◽  
Muscle Myosin

Isoforms of the smooth muscle myosin motor, SM1 and SM2, differ in length at the carboxy terminal tail region. Their proportion changes with development, hormonal status and disease, but their function is unknown. We developed mice carrying the myosin heavy chain (MyHC) transgenes SM1, cMyc-tagged SM1, SM2, and V5-tagged SM2, and all transgenes corresponded to the SMa NH2-terminal isoform. Transgene expression was targeted to smooth muscle by the smooth muscle α-actin promoter. Immunoblot analysis showed substantial expression of the cMyc-tagged SM1 and V5-tagged SM2 MyHC protein in aorta and bladder and transgene mRNA was expressed in mice carrying unlabeled SM1 or SM2 transgenes. Despite significant protein expression of tagged MyHCs we found only small changes in the SM1:SM2 protein ratio. Significant changes in functional phenotype were observed in mice carrying unlabeled SM1 or SM2 transgenes. Force in aorta and bladder was increased (72 ± 14%, 92 ± 11%) in SM1 and decreased to 57 ± 1% and 80 ± 3% in SM2 transgenic mice. SM1 transgenic bladders had faster (1.8 ± 0.3 s) and SM2 slower (7.1 ± 0.5 s) rates of force redevelopment following a rapid step shortening. We hypothesize that small changes in the SM1:SM2 ratio could be amplified if they are associated with changes in thick filament assembly and underlie the altered contractility. These data provide evidence indicating an in vivo function for the COOH-terminal isoforms of smooth muscle myosin and suggest that the SM1:SM2 ratio is tightly regulated in smooth muscle tissues.

Expression of Desmin and Smooth Muscle Myosin Heavy Chain in Dermatofibromas

2002 ◽  
Vol 126 (10) ◽  
pp. 1179-1183 ◽  
Author(s):  
Andrea K. Bruecks ◽  
Martin J. Trotter
Keyword(s):  
Smooth Muscle ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Smooth Muscle Actin ◽  
Smooth Muscle Myosin ◽  
Immunoperoxidase Staining ◽  
Muscle Actin ◽  
Muscle Myosin ◽  
Hematoxylin Eosin ◽  
Focal Expression

Abstract Background.—The histopathologic features of dermatofibroma vary remarkably, and this diversity may occasionally cause problems in differentiating between benign and malignant mesenchymal lesions, including smooth muscle neoplasms. Immunohistochemical stains are sometimes necessary to clarify the histogenesis of a lesion. Objective.—To evaluate dermatofibromas for expression of desmin and smooth muscle myosin heavy chain (SM-MHC) antigens, which are commonly used as evidence of smooth muscle differentiation. Methods.—We studied 100 consecutive cases of dermatofibroma using hematoxylin-eosin–stained sections and immunoperoxidase staining with antibodies against desmin, SM-MHC, and smooth muscle actin. Results.—We found focal positivity for desmin in 9 cases, and in 2 of these cases, at least 10% of lesional cells showed strong expression. We found focal staining for SM-MHC in 10 cases, and in 2 of these cases, at least 10% of the lesional cells were positive. Regions positive for desmin and/or SM-MHC did not show definite histologic features of myogenous differentiation on hematoxylin-eosin–stained sections. All dermatofibromas expressing desmin and SM-MHC were also strongly positive for smooth muscle actin. Conclusions.—About 10% of dermatofibromas show focal expression of desmin and SM-MHC, and this expression may be present in up to 10% to 15% of lesional cells. Thus, in dermal spindle cell lesions, focal expression of these muscle antigens, like that of smooth muscle actin, is not diagnostic of a smooth muscle tumor.

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