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Effect of nitric oxide on vascular smooth muscle cell proliferation and insulin-like growth factor binding protein expression
Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för molekylär och klinisk medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Linköpings universitet, Hälsouniversitetet.
(engelsk)Manuskript (preprint) (Annet vitenskapelig)
Abstract [en]

A possible interaction between nitric oxide (NO) and the insulin-like growth factor (IGF)-system was studied in cultured rat aortic smooth muscle cells. The NO-donor SNAP markedly inhibited basal and sernm-induced DNA synthesis while addition of L-NAME, an inhibitor of endogenous NO production, had no effect. L-NAME did also not significantly affect IGF-I, angiotensin II or TGF-ß1- induced effects on DNA synthesis. IGF-I was shown to stimulate the expression of IGFBP-4 mRNA, as measured by an RNase-protection assay, and angiotensin II inhibited expression of IGFBP-2 mRNA. Addition of L-NAME did not significantly change the effect of IGF-I or angiotensin II on IGFBP mRNA expression, neither did L-NAME or SNAP affect basal expression of IGFBP-2, -4 or -6 mRNA. In conclusion, we found no evidence for interaction of NO with the IGF-system in smooth muscle cells. Nitric oxide did not regulate the expression of IGFBPs and IGF-I-induced smooth muscle cell proliferation was not affected by inhibition of endogenous NO production.

HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-79729OAI: oai:DiVA.org:liu-79729DiVA, id: diva2:544038
Tilgjengelig fra: 2012-08-13 Laget: 2012-08-13 Sist oppdatert: 2012-08-13bibliografisk kontrollert
Inngår i avhandling
1. Action and interaction of growth factors and regulatory molecules in vascular cells: With special reference to the IGF-I-system
Åpne denne publikasjonen i ny fane eller vindu >>Action and interaction of growth factors and regulatory molecules in vascular cells: With special reference to the IGF-I-system
2000 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Vascular function is greatly influenced by growth factors and regulatory molecules that can interact with each other in a complex pattern in the vascular wall. In this thesis we studied how different substances of special interest in the pathogenesis of vascular disease interact and regulate each other's expressions in endothelial cells and vascular smooth muscle cells (VSMCs).

In VSMCs, angiotensin II was shown to delay PDGF-BB induced cell growth. This transient inhibitory effect of angiotensin II was mediated by the AT1-receptor, did not involve autocrine action of transforming growth factor-ß1 (TGF-ß1) and acted at a site downstream of PDGF-ß receptor phosphorylation.

The interaction of the insulin-like growth factor-system (IGF-system) with various growth factors, glucose and nitric oxide (NO) was studied in vascular cells. Vascular endothelial growth factor (VEGF) and transforming growth factor-ß1 (TGF-ß1) regulated the expression of insulin-like growth factor-binding proteins (IGFBPs) in large vessel endothelial cells in a way that might cause an increased bioavailability of IGF-I locally in the subendothelial space. Angiotensin II, IGF-I and insulin did not affect IGFBP expression in these cells. The expression of IGFBPs was studied for the first time in human micro vessel endothelial cells. No effect of high glucose treatment on IGFBP expression was seen in either large vessel endothelial cells or microvessel endothelial cells. A possible interaction between NO and the IGF-system was studied in VSMCs. IGF-I did not have any significant effect on NO production in VSMCs and neither exogenous nor endogenous NO had any effect on IGFBP expression.

In conclusion, we found that angiotensin II interacts with PDGF-BB in the regulation of VSMC growth. The IGF-system is regulated by VEGF and TGF-ß1 in endothelial cells while no effect of angiotensin II, IGF-I, insulin or high glucose was seen. We found no evidence for interaction of NO and the IGF-system in VSMCs.

sted, utgiver, år, opplag, sider
Linköping: Linköpings universitet, 2000. s. 69
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 637
HSV kategori
Identifikatorer
urn:nbn:se:liu:diva-25637 (URN)10011 (Lokal ID)91-7219-738-2 (ISBN)10011 (Arkivnummer)10011 (OAI)
Disputas
2000-09-22, Berzeliussalen, Universitetssjukhuset, Linköping, 09:00 (svensk)
Opponent
Tilgjengelig fra: 2009-10-08 Laget: 2009-10-08 Sist oppdatert: 2012-08-13bibliografisk kontrollert

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