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

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

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background: Several physiological adaptations occur in the respiratory muscles in rodent models of elastase-induced emphysema. Although the contractile properties of the diaphragm are altered in a way that suggests expression of slower isoforms of myosin heavy chain (MHC), it has been difficult to demonstrate a shift in MHCs in an animal model that corresponds to the shift toward slower MHCs seen in human emphysema. Methods: We sought to identify MHC and corresponding physiological changes in the diaphragms of rats with elastase-induced emphysema. Nine rats with emphysema and 11 control rats were studied 10 months after instillation with elastase. MHC isoform composition was determined by both reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry by using specific probes able to identify all known adult isoforms. Physiological adaptation was studied on diaphragm strips stimulated in vitro. Results: In addition to confirming that emphysematous diaphragm has a decreased fatigability, we identified a significantly longer time-to-peak-tension (63.9 ± 2.7 ms versus 53.9 ± 2.4 ms). At both the RNA (RT-PCR) and protein (immunocytochemistry) levels, we found a significant decrease in the fastest, MHC isoform (IIb) in emphysema. Conclusion: This is the first demonstration of MHC shifts and corresponding physiological changes in the diaphragm in an animal model of emphysema. It is established that rodent emphysema, like human emphysema, does result in a physiologically significant shift toward slower diaphragmatic MHC isoforms. In the rat, this occurs at the faster end of the MHC spectrum than in humans.

Original languageEnglish (US)
JournalRespiratory research
Volume4
DOIs
StatePublished - Feb 17 2003

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Physiological Adaptation
Myosin Heavy Chains
Pancreatic Elastase
Emphysema
Diaphragm
Protein Isoforms
Reverse Transcriptase Polymerase Chain Reaction
Rodentia
Animal Models
Immunohistochemistry
Respiratory Muscles
RNA-Directed DNA Polymerase

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

Kim, Dong Kwan ; Zhu, Jianliang ; Kozyak, Benjamin W. ; Burkman, James M. ; Rubinstein, Neal A. ; Lankford, Edward B. ; Stedman, Hansell H. ; Nguyen, Taitan ; Levine, Sanford ; Shrager, Joseph B. / Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema. In: Respiratory research. 2003 ; Vol. 4.
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title = "Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema",
abstract = "Background: Several physiological adaptations occur in the respiratory muscles in rodent models of elastase-induced emphysema. Although the contractile properties of the diaphragm are altered in a way that suggests expression of slower isoforms of myosin heavy chain (MHC), it has been difficult to demonstrate a shift in MHCs in an animal model that corresponds to the shift toward slower MHCs seen in human emphysema. Methods: We sought to identify MHC and corresponding physiological changes in the diaphragms of rats with elastase-induced emphysema. Nine rats with emphysema and 11 control rats were studied 10 months after instillation with elastase. MHC isoform composition was determined by both reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry by using specific probes able to identify all known adult isoforms. Physiological adaptation was studied on diaphragm strips stimulated in vitro. Results: In addition to confirming that emphysematous diaphragm has a decreased fatigability, we identified a significantly longer time-to-peak-tension (63.9 ± 2.7 ms versus 53.9 ± 2.4 ms). At both the RNA (RT-PCR) and protein (immunocytochemistry) levels, we found a significant decrease in the fastest, MHC isoform (IIb) in emphysema. Conclusion: This is the first demonstration of MHC shifts and corresponding physiological changes in the diaphragm in an animal model of emphysema. It is established that rodent emphysema, like human emphysema, does result in a physiologically significant shift toward slower diaphragmatic MHC isoforms. In the rat, this occurs at the faster end of the MHC spectrum than in humans.",
author = "Kim, {Dong Kwan} and Jianliang Zhu and Kozyak, {Benjamin W.} and Burkman, {James M.} and Rubinstein, {Neal A.} and Lankford, {Edward B.} and Stedman, {Hansell H.} and Taitan Nguyen and Sanford Levine and Shrager, {Joseph B.}",
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Kim, DK, Zhu, J, Kozyak, BW, Burkman, JM, Rubinstein, NA, Lankford, EB, Stedman, HH, Nguyen, T, Levine, S & Shrager, JB 2003, 'Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema', Respiratory research, vol. 4. https://doi.org/10.1186/rr196

Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema. / Kim, Dong Kwan; Zhu, Jianliang; Kozyak, Benjamin W.; Burkman, James M.; Rubinstein, Neal A.; Lankford, Edward B.; Stedman, Hansell H.; Nguyen, Taitan; Levine, Sanford; Shrager, Joseph B.

In: Respiratory research, Vol. 4, 17.02.2003.

Research output: Contribution to journalArticle

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T1 - Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema

AU - Kim, Dong Kwan

AU - Zhu, Jianliang

AU - Kozyak, Benjamin W.

AU - Burkman, James M.

AU - Rubinstein, Neal A.

AU - Lankford, Edward B.

AU - Stedman, Hansell H.

AU - Nguyen, Taitan

AU - Levine, Sanford

AU - Shrager, Joseph B.

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N2 - Background: Several physiological adaptations occur in the respiratory muscles in rodent models of elastase-induced emphysema. Although the contractile properties of the diaphragm are altered in a way that suggests expression of slower isoforms of myosin heavy chain (MHC), it has been difficult to demonstrate a shift in MHCs in an animal model that corresponds to the shift toward slower MHCs seen in human emphysema. Methods: We sought to identify MHC and corresponding physiological changes in the diaphragms of rats with elastase-induced emphysema. Nine rats with emphysema and 11 control rats were studied 10 months after instillation with elastase. MHC isoform composition was determined by both reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry by using specific probes able to identify all known adult isoforms. Physiological adaptation was studied on diaphragm strips stimulated in vitro. Results: In addition to confirming that emphysematous diaphragm has a decreased fatigability, we identified a significantly longer time-to-peak-tension (63.9 ± 2.7 ms versus 53.9 ± 2.4 ms). At both the RNA (RT-PCR) and protein (immunocytochemistry) levels, we found a significant decrease in the fastest, MHC isoform (IIb) in emphysema. Conclusion: This is the first demonstration of MHC shifts and corresponding physiological changes in the diaphragm in an animal model of emphysema. It is established that rodent emphysema, like human emphysema, does result in a physiologically significant shift toward slower diaphragmatic MHC isoforms. In the rat, this occurs at the faster end of the MHC spectrum than in humans.

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