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The cardiac protein αT-catenin contributes to chemical-induced asthma

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Abstract
Ten to 25% of adult asthma is occupational induced, a subtype caused by exposure to workplace chemicals. A recent genomewide association study identified single-nucleotide polymorphisms in the cardiac protein alpha T-catenin (alpha T-cat) that correlated with the incidence and severity of toluene diisocyanate (TDI) occupational asthma. alpha T-cat is a critical mediator of cell-cell adhesion and is predominantly expressed in cardiomyocytes, but its connection to asthma remains unknown. Therefore, we sought to determine the primary alpha T-cat-expressing cell type in the lung and its contribution to lung physiology in a murine model of TDI asthma. We show that alpha T-cat is expressed in lung within the cardiac sheath of pulmonary veins. Mechanically ventilated alpha T-cat knockout (KO) mice exhibit a significantly increased pressure-volume curve area compared with wild-type (WT) mice, suggesting that alpha T-cat loss affects lung hysteresis. Using a murine model of TDI asthma, we find that alpha T-cat KO mice show increased airway hyper-responsiveness to methacholine compared with WT mice. Bronchoalveolar lavage reveals only a mild macrophage-dominant inflammation that is not significantly different between WT and KO mice. These data suggest that alpha T-cat may contribute to asthma through a mechanism independent of inflammation and related to heart and pulmonary vein dysfunction.
Keywords
CTNNA3, GENE, DIISOCYANATE-INDUCED ASTHMA, MURINE MODEL, occupational asthma, lung hysteresis, cell-cell adhesion, alpha T-catenin

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MLA
Folmsbee, Stephen Sal et al. “The Cardiac Protein αT-catenin Contributes to Chemical-induced Asthma.” AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 308.3 (2015): L253–L258. Print.
APA
Folmsbee, S. S., Morales-Nebreda, L., van Hengel, J., Tyberghein, K., Van Roy, F., Budinger, G. S., Bryce, P. J., et al. (2015). The cardiac protein αT-catenin contributes to chemical-induced asthma. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 308(3), L253–L258.
Chicago author-date
Folmsbee, Stephen Sal, Luisa Morales-Nebreda, Jolanda van Hengel, Koen Tyberghein, Frans Van Roy, GR Scott Budinger, Paul J Bryce, and Cara J Gottardi. 2015. “The Cardiac Protein αT-catenin Contributes to Chemical-induced Asthma.” American Journal of Physiology-lung Cellular and Molecular Physiology 308 (3): L253–L258.
Chicago author-date (all authors)
Folmsbee, Stephen Sal, Luisa Morales-Nebreda, Jolanda van Hengel, Koen Tyberghein, Frans Van Roy, GR Scott Budinger, Paul J Bryce, and Cara J Gottardi. 2015. “The Cardiac Protein αT-catenin Contributes to Chemical-induced Asthma.” American Journal of Physiology-lung Cellular and Molecular Physiology 308 (3): L253–L258.
Vancouver
1.
Folmsbee SS, Morales-Nebreda L, van Hengel J, Tyberghein K, Van Roy F, Budinger GS, et al. The cardiac protein αT-catenin contributes to chemical-induced asthma. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY. 2015;308(3):L253–L258.
IEEE
[1]
S. S. Folmsbee et al., “The cardiac protein αT-catenin contributes to chemical-induced asthma,” AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, vol. 308, no. 3, pp. L253–L258, 2015.
@article{5878466,
  abstract     = {Ten to 25% of adult asthma is occupational induced, a subtype caused by exposure to workplace chemicals. A recent genomewide association study identified single-nucleotide polymorphisms in the cardiac protein alpha T-catenin (alpha T-cat) that correlated with the incidence and severity of toluene diisocyanate (TDI) occupational asthma. alpha T-cat is a critical mediator of cell-cell adhesion and is predominantly expressed in cardiomyocytes, but its connection to asthma remains unknown. Therefore, we sought to determine the primary alpha T-cat-expressing cell type in the lung and its contribution to lung physiology in a murine model of TDI asthma. We show that alpha T-cat is expressed in lung within the cardiac sheath of pulmonary veins. Mechanically ventilated alpha T-cat knockout (KO) mice exhibit a significantly increased pressure-volume curve area compared with wild-type (WT) mice, suggesting that alpha T-cat loss affects lung hysteresis. Using a murine model of TDI asthma, we find that alpha T-cat KO mice show increased airway hyper-responsiveness to methacholine compared with WT mice. Bronchoalveolar lavage reveals only a mild macrophage-dominant inflammation that is not significantly different between WT and KO mice. These data suggest that alpha T-cat may contribute to asthma through a mechanism independent of inflammation and related to heart and pulmonary vein dysfunction.},
  author       = {Folmsbee, Stephen Sal and Morales-Nebreda, Luisa and van Hengel, Jolanda and Tyberghein, Koen and Van Roy, Frans and Budinger, GR Scott and Bryce, Paul J and Gottardi, Cara J},
  issn         = {1040-0605},
  journal      = {AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY},
  keywords     = {CTNNA3,GENE,DIISOCYANATE-INDUCED ASTHMA,MURINE MODEL,occupational asthma,lung hysteresis,cell-cell adhesion,alpha T-catenin},
  language     = {eng},
  number       = {3},
  pages        = {L253--L258},
  title        = {The cardiac protein αT-catenin contributes to chemical-induced asthma},
  url          = {http://dx.doi.org/10.1152/ajplung.00331.2014},
  volume       = {308},
  year         = {2015},
}

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