Spontaneous expression of the c-sis gene and release of a platelet-derived growth factorlike molecule by human alveolar macrophages. Academic Article uri icon

Overview

MeSH

  • Chemotaxis
  • Cycloheximide
  • Hot Temperature
  • Humans
  • Hydrogen-Ion Concentration
  • RNA, Messenger
  • Radioimmunoassay
  • Transcription, Genetic
  • Trypsin

MeSH Major

  • Gene Expression Regulation
  • Lung Diseases
  • Platelet-Derived Growth Factor
  • Proto-Oncogenes
  • Pulmonary Alveoli

abstract

  • Alveolar macrophages from normal individuals and patients with interstitial lung diseases spontaneously expressed a 4.2-kilobase mRNA complementary to the c-sis gene, a proto-oncogene coding for one of the chains of platelet-derived growth factor (PDGF). Concomitantly, these cells released a mediator with the properties of PDGF, including: chemotactic factor for smooth muscle cells whose activity was resistant to heat and acid, but sensitive to reduction; mitogenic (competence) activity for fibroblasts; ability to compete with PDGF for its receptor; and precipitated by an anti-PDGF antibody. While blood monocytes did not contain c-sis mRNA transcripts, monocytes matured in vitro expressed c-sis, consistent with the concept that expression of c-sis occurs during the differentiation of monocytes into alveolar macrophages. Together with the known actions of PDGF, these observations suggest that the c-sis proto-oncogene and its PDGF product are part of the armamentarium available to the alveolar macrophages for normal lung defense and participation in lung inflammation.

publication date

  • July 1986

has subject area

  • Chemotaxis
  • Cycloheximide
  • Gene Expression Regulation
  • Hot Temperature
  • Humans
  • Hydrogen-Ion Concentration
  • Lung Diseases
  • Platelet-Derived Growth Factor
  • Proto-Oncogenes
  • Pulmonary Alveoli
  • RNA, Messenger
  • Radioimmunoassay
  • Transcription, Genetic
  • Trypsin

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC329531

Digital Object Identifier (DOI)

  • 10.1172/JCI112574

PubMed ID

  • 3722386

Additional Document Info

start page

  • 61

end page

  • 66

volume

  • 78

number

  • 1