Ontogeny and regulation of platelet-derived growth factor gene expression in distal fetal rat lung epithelial cells.

S. Buch, D. Jassal, I. Cannigia, J. Edelson, R. Han, J. Liu, K. Tanswell, M. Post

Research output: Contribution to journalArticle

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Abstract

Using flow cytometry, thymidine uptake into DNA, and expression of two growth-related genes, histone 3 and c-myc, we found an increase in the proportion of distal lung epithelial cells in the G0/G1 phase of the cell cycle with advancing gestation. Since our previous studies had demonstrated that platelet-derived growth factor (PDGF) is essential for the progression of these cells from the G0/G1 to the S phase of cell cycle, we investigated the gene and protein expression of PDGF-related genes (PDGF-A, PDGF-B, alpha-receptor, and beta-receptor) in distal fetal lung epithelial cells. The cells transcribed all the PDGF-related genes and translated the PDGF-A and PDGF-B mRNAs into protein, as demonstrated by immunocytochemistry and immunoprecipitation. To explore an autocrine role for PDGF in distal fetal lung epithelial cells, intervention studies using PDGF-A and -B chain-specific antisense oligodeoxynucleotides (ODN) were carried out. Antisense PDGF-B ODN, but not antisense PDGF-A ODN, significantly reduced the DNA synthesis of these cells. The inhibitory effect of antisense PDGF-B ODN on DNA synthesis was reversed by the addition of exogenous PDGF-BB, which supports an autocrine role in the DNA synthesis of these cells. We also examined the expression of PDGF genes in distal fetal lung epithelial cells during late gestation. PDGF-A chain and beta-receptor gene expressions declined with advancing gestation, whereas expression of message for PDGF-B chain and alpha-receptor increased. The increases in message for PDGF-B chain and alpha-receptor with advancing gestation were due to a greater rate of transcription, whereas the developmental decrease of PDGF-A chain and beta-receptor mRNAs was caused by a decrease in RNA stability. Taken together with the ODN data, these results suggest that the G0/G1 cell cycle arrest of distal lung epithelial cells during late fetal gestation is due to a decrease in PDGF beta-receptor expression by the cells.

Original languageEnglish (US)
Pages (from-to)251-261
Number of pages11
JournalAmerican journal of respiratory cell and molecular biology
Volume11
Issue number3
DOIs
StatePublished - Sep 1994

Fingerprint

Proto-Oncogene Proteins c-sis
Platelet-Derived Growth Factor
Gene expression
Oligodeoxyribonucleotides
Rats
Epithelial Cells
Gene Expression
Lung
Genes
Cells
Pregnancy
DNA
Platelet-Derived Growth Factor beta Receptor
Messenger RNA
Platelet-Derived Growth Factor alpha Receptor
Flow cytometry
G1 Phase Cell Cycle Checkpoints
cdc Genes
Cell Cycle Resting Phase
Cell Cycle Proteins

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

Cite this

Ontogeny and regulation of platelet-derived growth factor gene expression in distal fetal rat lung epithelial cells. / Buch, S.; Jassal, D.; Cannigia, I.; Edelson, J.; Han, R.; Liu, J.; Tanswell, K.; Post, M.

In: American journal of respiratory cell and molecular biology, Vol. 11, No. 3, 09.1994, p. 251-261.

Research output: Contribution to journalArticle

Buch, S. ; Jassal, D. ; Cannigia, I. ; Edelson, J. ; Han, R. ; Liu, J. ; Tanswell, K. ; Post, M. / Ontogeny and regulation of platelet-derived growth factor gene expression in distal fetal rat lung epithelial cells. In: American journal of respiratory cell and molecular biology. 1994 ; Vol. 11, No. 3. pp. 251-261.
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