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IFN gamma regulates PDGF-receptor alpha expression in macrophages, THP-1 cells, and arterial smooth muscle cells
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden / Wallenberg Laboratory, Sahlgrenska University Hospital, Göteborg, Sweden.
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.
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2006 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 184, no 1, 39-47 p.Article in journal (Refereed) Published
Abstract [en]

The recruitment of monocyte-derived macrophages (MDMs) and arterial smooth muscle cells (ASMCs) contributes to inflammation and development of intimal hyperplasia during atherosclerosis. Platelet-derived growth factor (PDGF) is a potent mitogen for SMC, signalling through PDGF-receptor subunits alpha (Ralpha) and beta (Rbeta). We have previously found that interferon gamma (IFNgamma) upregulates PDGF-Ralpha mRNA expression in human MDM (hMDM) which causes an increased migration towards PDGF. In the present study, we found that IFNgamma mediated an upregulation of PDGF-Ralpha mRNA also in THP-1 cells. The induction of PDGF-Ralpha in both hMDM and THP-1 cells was caused by STAT1 binding to the PDGF-Ralpha promoter. In human ASMCs, IFNgamma again stimulated a transient STAT1-binding to the PDGF-Ralpha promoter. However, this was not followed by an upregulation of PDGF-Ralpha mRNA. IFNgamma-stimulation resulted in augmented expression of PDGF-Ralpha protein in differentiated hMDM. Early hMDM only expressed an immature and not fully glycosylated form of the PDGF-Ralpha protein. In contrast, THP-1 cells did not synthesize PDGF-Ralpha protein, implying further posttranscriptional inhibition. Our results contribute to a better understanding of the complex regulation of PDGF-Ralpha expression and how proinflammatory factors may contribute to PDGF-related hyperplasia in vascular diseases.

Place, publisher, year, edition, pages
Elsevier, 2006. Vol. 184, no 1, 39-47 p.
Keyword [en]
PDGF, Receptor, IFNγ, Atherosclerosis, Transcriptional regulation, STAT
National Category
Other Basic Medicine
Research subject
Medical sciences
Identifiers
URN: urn:nbn:se:his:diva-11384DOI: 10.1016/j.atherosclerosis.2005.03.026ISI: 000234730100006PubMedID: 15871904Scopus ID: 2-s2.0-28344447320OAI: oai:DiVA.org:his-11384DiVA: diva2:847234
Available from: 2015-08-19 Created: 2015-08-19 Last updated: 2016-04-12Bibliographically approved

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