Retinoic acid-receptor activation of SP-B gene transcription in respiratory epithelial cells

Cong Yan, Manely Ghaffari, Jeffrey A. Whitsett, Xin Zeng, Zvjezdana Sever, Sui Lin

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

Retinoids are known to play important roles in organ development of the lung. Retinoids exert their activity by modulating the expression of numerous genes, generally influencing gene transcription, in target cells. In the present work, the mechanism by which retinoic acid (RA) regulates surfactant protein (SP) B expression was assessed in vitro. RA (9-cis-RA) enhanced SP-B mRNA in pulmonary adenocarcinoma cells (H441 cells) and increased transcriptional activity of the SP-B promoter in both H441 and mouse lung epithelial cells (MLE-15). Cotransfection of H441 cells with retinoid nuclear receptor (RAR)-α, -β, and -γ and retinoid X receptor (RXR)-γ further increased the response of the SP-B promoter to RA. Treatment of H441 cells with RA increased immunostaining for the SP-B proprotein and increased the number of cells in which the SP-B proprotein was detected. An RA responsive element mediating RA stimulation of the human SP-B promoter was identified. RAR-α and -γ and RXR-α but not RAR-β or RXR-β and -γ were detected by immunohistochemical analysis of H441 cells. RA, by activating RAR activity, stimulated the transcription and synthesis of SP-B in pulmonary adenocarcinoma cells.

Original languageEnglish (US)
Pages (from-to)L239-L246
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume275
Issue number2 19-2
StatePublished - Aug 1 1998
Externally publishedYes

Keywords

  • Glucocorticoid receptor
  • Surfactant protein B
  • Thyroid transcription factor-1

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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