Search for: [Abstract = "The model used in the study – mice with deletion of RXRα gene in hepatocytes \(hRXR ko\) made it possible to investigate the effect of metabolic disturbances \- higher cholesterol and leptin level in the blood \(with normal insulin level and improved glucose tolerance\) on angiogenesis.In order to expose metabolic syndrome parameters, hRXR ko and wild type mice were fed either high fat diet or control, standard diet for 7 weeks. During feeding mice were weighted and biochemical parametres were measured in the blood. To estimate angiogenic response, in 6th week of feeding, animals were subcutaneously injected with matrigel containing bFGF \[25nM\] for 6 days. Angiogenesis was assumed in matrigel paraffin sections stained immunohistochemically against CD31 antigen. In matrigel plug cells, gene expression was also analysed.High fat diet feeding resulted in higher cholesterol and leptin level in serum and also in the tendency to decreased angiogenic response \(number of vessels with lumen\) in hRXR ko mice. Gene expression analysis in matrigel plugs from hRXR ko mice showed inhibition of genes related to angiogenesis as well as activation of\: apoptosis inducers, proinflammatory genes and genes connected with initial steps of adipogenesis. Presented results suggest that angiogenic response in hRXR ko mice is mainly regulated by disturbances of lipid metabolism, but not by proangiogenic leptin. The reason of weaker angiogenic response in these mice could be activation of apoptosis which is caused on the one hand, by lipotoxicity in cells participating in neovascularisation and on the other hand, by adipogenesis induction"]

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