Inhibition of TGF-α gene expression by vitamin A in airway epithelium

Lisa Miller, Yu Hua Zhao, Reen Wu

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The autocrine/paracrine growth mechanism has been implicated in the regulation of bronchial epithelial cell proliferation. By inhibiting the expression of the transforming growth factor-α (TGF-α) gene product, vitamin A is able to suppress the proliferation of tracheobronchial epithelial cells in culture. Similar repressions in TGF-α mRNA levels by retinol were observed in airway explant cultures and in a cell line immortalized from normal human bronchial epithelial cells. Both the nuclear run-on transcriptional assay and the transfection study with the chimeric construct of the TGF-α promoter and chloramphenicol acetyltransferase reporter gene partly suggest a transcriptional down-regulation mechanism of TGF-α gene expression by the retinol treatment; however, this inhibition at the transcriptional level cannot account for the total inhibition at the mRNA level. These results suggest that a downregulation of the expression of the TGF-α gene at the transcriptional and post-transcriptional levels by vitamin A may precede the essential event associated with the homeostasis of normal conducting airway epithelium.

Original languageEnglish (US)
Pages (from-to)1429-1435
Number of pages7
JournalJournal of Clinical Investigation
Volume97
Issue number6
StatePublished - Mar 15 1996

Fingerprint

Transforming Growth Factors
Vitamin A
Epithelium
Gene Expression
Epithelial Cells
Down-Regulation
Messenger RNA
Chloramphenicol O-Acetyltransferase
Reporter Genes
Genes
Transfection
Homeostasis
Cell Culture Techniques
Cell Proliferation
Cell Line
Growth

Keywords

  • autocrine/paracrine
  • gene expression
  • growth factor
  • retinoids
  • transcriptional regulation

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Inhibition of TGF-α gene expression by vitamin A in airway epithelium. / Miller, Lisa; Zhao, Yu Hua; Wu, Reen.

In: Journal of Clinical Investigation, Vol. 97, No. 6, 15.03.1996, p. 1429-1435.

Research output: Contribution to journalArticle

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