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Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair.

Publication ,  Journal Article
Zhao, Y; Gilmore, BJ; Young, SL
Published in: Am J Physiol
August 1997

Lung injury and repair processes involve many cellular activities, including cell growth, differentiation, and remodeling of extracellular matrix components. Transforming growth factor-beta (TGF-beta) is a major class of signaling peptide growth factors regulating these cellular activities. Type I (T beta RI) and type II (T beta RII) receptors for TGF-beta are transmembrane serine/threonine kinases that are essential for TGF-beta signaling. To gain insight into the possible molecular mechanisms of lung injury and repair, we investigated the expression of T beta RI and T beta RII in an acute hyperoxia-induced model of lung injury and repair. Localization of message expression of T beta RI and T beta RII in oxygen-exposed rat lung tissue was analyzed by using in situ hybridization. T beta RI mRNA expression was found in the interstitium, capillaries, and the alveolar septa of rat lungs exposed for 60 h to 100% oxygen. The distribution of T beta RII mRNA in oxygen-exposed rat lung tissue overlapped the localization of T beta RI mRNA. Temporal changes of T beta RI and T beta RII mRNA expressions in rat lung during hyperoxic exposure and repair were examined by Northern analysis. We found that expression of T beta RI was upregulated in adult rats undergoing prolonged exposure to 100% oxygen, and the increase of T beta RI expression persisted during 2 wk of repair of lung injury. The pattern of T beta RII expression during hyperoxic exposure and repair was distinct from that of T beta RI. The expression of T beta RII increased with a peak at 3 days postexposure and then declined after 7 days of repair. Changes of T beta RI and T beta RII protein expressions in rat lung during hyperoxic exposure and repair were examined further by Western blot analysis, which correlated with the mRNA expression. The results suggest that T beta RI and T beta RII may play important roles during the lung injury and repair by mediating signaling activity of TGF-beta and may regulate interactions between the mesenchyme and the epithelium.

Duke Scholars

Published In

Am J Physiol

DOI

ISSN

0002-9513

Publication Date

August 1997

Volume

273

Issue

2 Pt 1

Start / End Page

L355 / L362

Location

United States

Related Subject Headings

  • Wound Healing
  • Time Factors
  • Receptors, Transforming Growth Factor beta
  • Rats, Sprague-Dawley
  • Rats
  • RNA, Messenger
  • Lung
  • In Situ Hybridization
  • Hyperoxia
  • Cardiovascular System & Hematology
 

Citation

APA
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ICMJE
MLA
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Zhao, Y., Gilmore, B. J., & Young, S. L. (1997). Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair. Am J Physiol, 273(2 Pt 1), L355–L362. https://doi.org/10.1152/ajplung.1997.273.2.L355
Zhao, Y., B. J. Gilmore, and S. L. Young. “Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair.Am J Physiol 273, no. 2 Pt 1 (August 1997): L355–62. https://doi.org/10.1152/ajplung.1997.273.2.L355.
Zhao Y, Gilmore BJ, Young SL. Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair. Am J Physiol. 1997 Aug;273(2 Pt 1):L355–62.
Zhao, Y., et al. “Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair.Am J Physiol, vol. 273, no. 2 Pt 1, Aug. 1997, pp. L355–62. Pubmed, doi:10.1152/ajplung.1997.273.2.L355.
Zhao Y, Gilmore BJ, Young SL. Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair. Am J Physiol. 1997 Aug;273(2 Pt 1):L355–L362.

Published In

Am J Physiol

DOI

ISSN

0002-9513

Publication Date

August 1997

Volume

273

Issue

2 Pt 1

Start / End Page

L355 / L362

Location

United States

Related Subject Headings

  • Wound Healing
  • Time Factors
  • Receptors, Transforming Growth Factor beta
  • Rats, Sprague-Dawley
  • Rats
  • RNA, Messenger
  • Lung
  • In Situ Hybridization
  • Hyperoxia
  • Cardiovascular System & Hematology