Elastin gene expression is upregulated during pulmonary fibrosis

Connect Tissue Res. 1999;40(2):145-53. doi: 10.3109/03008209909029110.


Elastin is a chief component of lung interstitium, and it is central to lung morphology and function. Efforts to understand the pathogenesis of pulmonary fibrosis have focused primarily upon collagen turnover in the lung; few studies have focused on elastin. In this study, we examined steady-state elastin mRNA levels after lung injury in the mouse induced by (1) butylated hydroxytoluene (BHT) which causes acute lung injury with recovery, (2) BHT + 70% O2 (fibrosis), or (3) 70% O2. Total lung elastin mRNA increased 70-80-fold on d10-14 after BHT/O2, but was unchanged after BHT or O2 alone. In situ hybridization studies localized elastin mRNA to cells in the muscularis of conducting airways and to scattered interstitial cells in fibrotic foci. Elastic fiber morphology was markedly distorted after BHT/O2. Thus, marked upregulation of elastin gene expression is correlated with the histopathology of fibrotic lung disease.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blotting, Northern
  • Butylated Hydroxytoluene
  • Elastin / biosynthesis
  • Elastin / genetics*
  • Gene Expression*
  • In Situ Hybridization
  • Lung / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Pulmonary Fibrosis / chemically induced
  • Pulmonary Fibrosis / genetics*
  • Pulmonary Fibrosis / metabolism
  • RNA, Messenger / biosynthesis*
  • Up-Regulation


  • RNA, Messenger
  • Butylated Hydroxytoluene
  • Elastin