Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema

Kim, Dong Kwan; Zhu, Jie; Kozyak, Benjamin W; Burkman, James M.; Rubinstein, Neal A.; Lankford, Edward B.; Stedman, Hansell H.; Nguyen, Taitan; Levine, Stephen B.; Shrager, Joseph B.

doi:10.1186/rr196

Cited by 27 publications

(23 citation statements)

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“…Changes in type IIB fibers are sometimes present, but these represent 5-10% of the total fibers in the rodent diaphragm and probably are nonexistent in the human diaphragm. The lack of consistent shifts in fiber populations is also consistent with one study by Kim et al (36) that showed only minor changes in the proportions of MHC isoforms in the rat emphysema model.…”

Section: Changes In Fiber Phenotype and Sizesupporting

confidence: 79%

“…In animal models of elastase-induced emphysema, after periods of 6 mo or more, most studies have found that changes in fiber distributions between type I, IIA, IIB, and IIX are modest and quite variable (22,31,32,36,43,44,49,52,85), as summarized in Table 1. None have found a significant elevation in the proportion of type I fibers, and there has been only one report of significant increases in the proportion of type IIA fibers (49), with an accompanying reduction in IIX fibers.…”

Section: Changes In Fiber Phenotype and Sizementioning

confidence: 99%

“…Whereas Marchand et al (49) found a significant reduction of type I fiber CSA (ϳ17%), this has not been a typical finding (Table 1). One study found an elevation in the fiber areas of type IA fibers (52), but a more typical response has been a general reduction in the size of large glycolytic fibers (22) or, specifically, type IIX (36,49).…”

Section: Changes In Fiber Phenotype and Sizementioning

confidence: 99%

“…In most studies of rat or hamster elastase-induced emphysema, there is little or no biologically significant reduction in maximum specific force (Ͻ10% change) of muscle bundles or individual fibers (20,21,31,36,49,85), as summarized in Table 1. The largest exceptions to this are the work of Lewis et al (43), who showed reductions in in vitro specific force of Ͼ20%, and Huenks et al (32), who demonstrated reductions of ϳ14%.…”

Section: Changes In Specific Forcementioning

confidence: 99%

“…This would be in agreement with the study by that has shown shorter sarcomeres in the diaphragm of COPD patients. Thus the area remains unresolved.In most studies of rat or hamster elastase-induced emphysema, there is little or no biologically significant reduction in maximum specific force (Ͻ10% change) of muscle bundles or individual fibers (20,21,31,36,49,85), as summarized in Table 1. The largest exceptions to this are the work of Lewis et al.…”

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confidence: 99%

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Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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Clanton TL, Levine S. Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation? J Appl Physiol 107: 324 -335, 2009. First published April 9, 2009 doi:10.1152/japplphysiol.00173.2009.-The diaphragm and other respiratory muscles undergo extensive remodeling in both animal models of emphysema and in human chronic obstructive pulmonary disease, but the nature of the remodeling is different in many respects. One common feature is a shift toward improved endurance characteristics and increased oxidative capacity. Furthermore, both animals and humans respond to chronic hyperinflation by diaphragm shortening. Although in rodent models this clearly arises by deletion of sarcomeres in series, the mechanism has not been proven conclusively in human chronic obstructive pulmonary disease. Unique characteristics of the adaptation in human diaphragms include shifts to more predominant slow, type I fibers, expressing slower myosin heavy chain isoforms, and type I and type II fiber atrophy. Although some laboratories report reductions in specific force, this may be accounted for by decreases in myosin heavy chain content as the muscles become more oxidative and more efficient. More recent findings have reported reductions in Ca 2ϩ sensitivity and reduced myofibrillar elastic recoil. In contrast, in rodent models of disease, there is no consistent evidence for loss of specific force, no consistent shift in fiber populations, and atrophy is predominantly seen only in fast, type IIX fibers. This review challenges the hypothesis that the adaptations in human diaphragm represent a form of dysfunction, secondary to systemic disease, and suggest that most findings can as well be attributed to adaptive processes of a complex muscle responding to unique alterations in its working environment. diaphragm; fiber type; sarcomere; skeletal muscle; emphysema THIS REVIEW IS INTENDED TO bring readers up to date with accumulating evidence that the diaphragm undergoes remarkable adaptations to chronic hyperinflation and chronic lung obstruction. Some of these adaptations are expected, based on well known responses of limb muscle to chronic changes in length and mechanical load, but others appear to be surprisingly unique, revealing aspects of muscle plasticity and pathology that are not anticipated from known basic science concepts. We will concentrate this review on what has been observed, primarily at the muscle fiber level in both animals and humans, with primary emphasis on the diaphragm. There have been several excellent previous reviews of this area, and the reader is encouraged to refer to these (13,41,58,65,66). Where possible, we will attempt to complement, update, and at times challenge current concepts with the purpose of furthering dialogue and promoting further inquiry. LENGTH PLASTICITYThe diaphragm, like all other muscles, exhibits a characteristic length-tension relationship analogous to the Frank-Starling curve for the heart. As length is increased in the relaxed muscle, a passive length-tension cu...

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Section: Changes In Fiber Phenotype and Sizesupporting

confidence: 79%

Section: Changes In Fiber Phenotype and Sizementioning

confidence: 99%

Section: Changes In Fiber Phenotype and Sizementioning

confidence: 99%

Section: Changes In Specific Forcementioning

confidence: 99%

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confidence: 99%

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Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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Lack of association of IL-12 p40 gene polymorphism with peptic ulcer disease

García-González¹,

Lanas²,

Wu³

et al. 2005

Human Immunology

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A review of metabolomics approaches and their application in identifying causal pathways of childhood asthma

Turi

Romick-Rosendale

Ryckman

et al. 2018

Journal of Allergy and Clinical Immunology

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Because asthma is a disease that results from host-environment interactions, an approach that allows assessment of the effect of the environment on the host is needed to understand the disease. Metabolomics has appealing potential as an application to study pathways to childhood asthma development. The objective of this review is to provide an overview of metabolomics methods and their application to understanding host-environment pathways in asthma development. We reviewed recent literature on advances in metabolomics and their application to study pathways to childhood asthma development. We highlight the (1) potential of metabolomics in understanding the pathogenesis of disease and the discovery of biomarkers; (2) choice of metabolomics techniques, biospecimen handling, and data analysis; (3) application to studying the role of the environment on asthma development; (4) review of metabolomics applied to the outcome of asthma; (5) recommendations for application of metabolomics-based -omics data integration in understanding disease pathogenesis; and (6) limitations. In conclusion, metabolomics allows use of biospecimens to identify useful biomarkers and pathways involved in disease development and subsequently to inform a greater understanding of disease pathogenesis and endotypes and prediction of the clinical course of childhood asthma phenotypes.

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Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema

Cited by 27 publications

References 52 publications

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Lack of association of IL-12 p40 gene polymorphism with peptic ulcer disease

A review of metabolomics approaches and their application in identifying causal pathways of childhood asthma

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