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ROCK insufficiency attenuates ozone-induced airway hyperresponsiveness in mice.

David I Kasahara1, Joel A Mathews2, Chan Y Park2

  • 1Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts; and dkasahar@hsph.harvard.edu.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|August 16, 2015
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Summary

Ozone exposure increases airway hyperresponsiveness (AHR). This study shows that Rho kinase (ROCK) isoforms ROCK1 and ROCK2 are crucial for ozone-induced AHR, with ROCK2 playing a key role downstream of inflammation.

Keywords:
bronchoalveolar lavagefasudilhyaluronaninflammationosteopontin

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Area of Science:

  • Pulmonary Medicine
  • Cellular Biology
  • Toxicology

Background:

  • Ozone exposure is a known cause of airway hyperresponsiveness (AHR) and lung inflammation.
  • Rho kinase (ROCK) is a critical enzyme regulating smooth muscle contraction and inflammatory cell movement.
  • The specific roles of ROCK isoforms, ROCK1 and ROCK2, in ozone-induced AHR are not fully understood.

Purpose of the Study:

  • To investigate the contribution of ROCK1 and ROCK2 isoforms to the development of ozone-induced AHR.
  • To elucidate the mechanisms by which ROCK isoforms mediate airway inflammation and hyperresponsiveness following ozone exposure.

Main Methods:

  • Exposure of wild-type, ROCK1(+/-), and ROCK2(+/-) mice to air or ozone (2 ppm for 3 hours).
  • Assessment of airway hyperresponsiveness, bronchoalveolar lavage (BAL) inflammatory cell counts, and specific molecular markers (hyaluronan, IL-17A, osteopontin, TNFα).
  • Administration of ROCK inhibitors (fasudil, SR3677) and evaluation of their effects on AHR and airway smooth muscle contraction.

Main Results:

  • ROCK1 or ROCK2 haploinsufficiency significantly reduced ozone-induced AHR, with ROCK2 haploinsufficiency showing a greater effect.
  • Ozone-induced increases in BAL hyaluronan were reduced in ROCK1(+/-) mice, but not ROCK2(+/-) mice.
  • ROCK2 expression increased following ozone exposure, and a ROCK2 inhibitor reduced contractile forces in human airway smooth muscle cells.

Conclusions:

  • Ozone-induced AHR is dependent on ROCK activity.
  • ROCK1 may contribute to ozone-induced AHR via hyaluronan pathways.
  • ROCK2 plays a critical role downstream of inflammation, primarily in mediating airway smooth muscle contraction in response to ozone.