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Biology of vascular endothelium isolated from transgenic mice YAC67 and YAC84 -mouse models for Down syndrome

Abstract : GIRK2 is located on chromosome 21, which trisomy is the cause of Down syndrome (DS). In DS, among other features, proportions of T lymphocytes subpopulations are altered and number of circulating B cells are decreased. We hypothesized that it is due to the disturbed control of homing/recirculation of lymphocytes by endothelial cells (ECs). ECs constitute the vessel wall, achieve the neovascularisation, interact with circulating cells, initiate the adhesion process thus, immunological response. To assess the GIRK2 gene influence on the function of ECs, an in vitro cellular model was established. ECs lines were established from bone marrow, thymus, peripheral lymph nodes, Peyer’s patches and brain from transgenic mice with additional copies of the gene and from normal control mice. Endothelium biology was investigated in the aspect of adhesion molecules as well as processes of adhesion and angiogenesis. ECs from transgenic mice have altered levels of CD29, CD34, their adhesive properties towards lymphoid cells are affected and their angiogenic properties are drastically different. cDNA microarray display for the gene expression pattern of ECs from transgenic mice showed that among adhesion molecules, chemokines, chemokine receptors, VEGFs and VEGFs receptors, more than one fourth of the mRNA was significantly modified compared to controls. Presented results give clear evidence that GIRK2 gene can influence the function of endothelial cells in DS patients.
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Submitted on : Friday, September 24, 2010 - 10:51:15 AM
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  • HAL Id : tel-00520763, version 1


Magdelena Tomczyńska. Biology of vascular endothelium isolated from transgenic mice YAC67 and YAC84 -mouse models for Down syndrome. Agricultural sciences. Université d'Orléans, 2009. English. ⟨NNT : 2009ORLE2067⟩. ⟨tel-00520763⟩



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