Obiekt

Tytuł: Angiogenesis in model of metabolic syndrome in mice with deficiency of retinoic acid receptor gene (RXR alfa) in hepatocytes

Abstrakt:

The model used in the study – mice with deletion of RXRα gene in hepatocytes (hRXRα 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, hRXRα 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 hRXRα ko mice. Gene expression analysis in matrigel plugs from hRXRα 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 hRXRα 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

Miejsce wydania:

Kraków

Stopień studiów:

2 - studia doktoranckie

Dyscyplina:

biochemia

Instytucja nadająca tytuł:

Wydział Lekarski

Promotor:

Dembińska-Kieć, Aldona

Data wydania:

2011

Identyfikator:

oai:dl.cm-uj.krakow.pl:3478

Sygnatura:

ZB-116986

Język:

pol

Prawa dostępu:

nieograniczony

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Data ostatniej modyfikacji:

26 cze 2023

Data dodania obiektu:

11 mar 2013

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1 597

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http://dl.cm-uj.krakow.pl:8080/publication/3478

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Nazwa wydania Data
ZB-116986 26 cze 2023
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