Document Detail

Hypoxia enhances cellular proliferation and inositol 1,4, 5-triphosphate generation in fibroblasts from bovine pulmonary artery but not from mesenteric artery.
MedLine Citation:
PMID:  9847264     Owner:  NLM     Status:  MEDLINE    
When pulmonary hypertension occurs in the face of hypoxia there is remodeling of all three layers of the pulmonary vessels, but in particular, there is an increase in number of adventitial fibroblasts. Hypoxia causes vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. We hypothesized that there are fundamental differences in oxygen sensing and cell signaling between systemic and pulmonary artery cells in response to hypoxia. Here, we determined the effect of hypoxia either alone or in combination with known growth factors such as serum, endothelin-1 (ET-1), and platelet-derived growth factor (PDGF) on the proliferative responses of bovine pulmonary artery and mesenteric artery fibroblasts. Fibroblasts were obtained from primary cultures. Growth was assessed by [3H]thymidine incorporation. Inositol 1,4,5-triphosphate (IP3) generation was measured using a competitive binding assay. Hypoxia alone increased proliferation of pulmonary artery fibroblasts (611 +/- 24%), but not in those from the mesentery. Furthermore, hypoxia had the effect of increasing the replicative response of pulmonary fibroblasts to serum and PDGF, but no change was observed in the mesenteric cells. ET-1 had no effect on growth of either cell type. PDGF gave rise to a significant elevation in IP3 production under hypoxic conditions in the pulmonary artery cells (234%), but not in the mesenteric cells. ET-1 caused no change in IP3 production in any cell type. These data suggest that hypoxia sensitizes pulmonary artery fibroblasts to the proliferative effect of mitogens through a pathway that is not present, or is present but repressed, in the mesenteric cells.
D J Welsh; P Scott; R Plevin; R Wadsworth; A J Peacock
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  158     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  1998 Dec 
Date Detail:
Created Date:  1999-01-25     Completed Date:  1999-01-25     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1757-62     Citation Subset:  AIM; IM    
Pulmonary Vascular Unit, Department of Respiratory Medicine, Western Infirmary, and Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, United Kingdom.
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MeSH Terms
Analysis of Variance
Anoxia / metabolism,  pathology*,  physiopathology
Cell Communication
Cell Division
Cells, Cultured
Elastic Tissue / metabolism,  pathology
Endothelin-1 / pharmacology
Fibroblasts / drug effects,  metabolism,  pathology*
Hypertension, Pulmonary / metabolism,  pathology
Inositol 1,4,5-Trisphosphate / biosynthesis*
Mesenteric Arteries / drug effects,  metabolism,  pathology*
Mitogens / pharmacology
Platelet-Derived Growth Factor / pharmacology
Pulmonary Artery / drug effects,  metabolism,  pathology*
Radiopharmaceuticals / diagnostic use
Thymidine / diagnostic use,  metabolism
Tritium / diagnostic use
Vasoconstriction / physiology
Vasodilation / physiology
Reg. No./Substance:
0/Endothelin-1; 0/Mitogens; 0/Platelet-Derived Growth Factor; 0/Radiopharmaceuticals; 10028-17-8/Tritium; 50-89-5/Thymidine; 85166-31-0/Inositol 1,4,5-Trisphosphate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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