Sökning: onr:"swepub:oai:DiVA.org:his-11410" >
Effect of phenotype...
-
Krettek, Alexandra,1968-Wellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden / Wallenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden
(författare)
Effect of phenotype on the transcription of the genes for platelet-derived growth factor (PDGF) isoforms in human smooth muscle cells, monocyte-derived macrophages, and endothelial cells in vitro
- Artikel/kapitelEngelska1997
Förlag, utgivningsår, omfång ...
-
Lippincott Williams & Wilkins,1997
-
printrdacarrier
Nummerbeteckningar
-
LIBRIS-ID:oai:DiVA.org:his-11410
-
https://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11410URI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:art swepub-publicationtype
Anmärkningar
-
Proliferation of arterial smooth muscle cells (ASMCs) contributes considerably to enlargement of the arterial wall during atherosclerosis. The platelet-derived growth factor (PDGF) is a well-known mitogen and chemoattractant for ASMCs. Quantitative reverse transcription-polymerase chain reaction showed that cells appearing in atherosclerotic lesions, such as ASMCs, endothelial cells, and monocytes/macrophages, expressed mRNAs for both PDGF A and B chains in vitro, with the highest expression in endothelial cells. On proliferation, ASMCs and endothelial cells upregulated PDGF A mRNA. Differentiation of macrophages increased the amount of both mRNAs. Thus, the regulation of PDGF A- and B-chain expression depends on cell types and phenotypic states of the cells, which have also been found in vivo in human atherosclerotic lesions. PDGF A can be produced as short and long isoforms. The latter binds with high affinity to glycosaminoglycans. Irrespective of phenotype, only the minor part of total PDGF A mRNA consisted of the long variant in ASMCs, while endothelial cells produced 40% of total PDGF A as the long form. The differentiation of macrophages increased the production of the long PDGF A mRNA from 10% to 40%. Thus, increasing numbers of stimulated cells in the atherosclerotic lesion may increase the transcription of PDGF isoforms, and particularly of the long PDGF A isoform. Together with increasing amounts of ASMC-derived proteoglycans in developing lesions, this may contribute to accumulation of PDGF in the arterial wall matrix, resulting in prolonged stimulation of ASMCs.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Fager, G.Wellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden
(författare)
-
Lindmark, H.Wellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden
(författare)
-
Simonson, C.Wellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden
(författare)
-
Lustig, F.Wellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden
(författare)
-
Wellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden / Wallenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, SwedenWellenberg Lab. for Cardiovasc. Res., Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Arteriosclerosis, Thrombosis and Vascular Biology: Lippincott Williams & Wilkins17:11, s. 2897-29031079-56421524-4636
Internetlänk
Hitta via bibliotek
Till lärosätets databas