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LDLR-DEFICIENT MICE
Poster - BASIC SCIENCE - Animal Models Abstract: P181 Citation: Atherosclerosis Supplement 2009, Vol. 10, Issue 2
ENDOGLIN EXPRESSION IN ATHEROGENESIS AND AFTER ATORVASTATIN TREATMENT IN APOE/LDLR-DEFICIENT MICE P Nachtigal1, L Vecerova1, S Micuda2, E Brcakova2, D Solichova3 1
Biological and Medical Sciences, Charles University in Prague, Faculty of Pharmacy, Hradec Kralove; 2Pharmacology, Charles University in Prague, Faculty of Medicine, Hradec Kralove; 3 Metabolic Care and Gerontology, Charles University Medical School and Teaching Hospital, Hradec Kralove Objectives: Endoglin (CD 105) has been demonstrated to affect TGF-ȕ signaling and eNOS expression by affecting SMAD2 protein in vitro. Thus, in this study we wanted to elucidate whether endoglin is co-expressed with SMAD2 and eNOS in vivo and whether it is affected by the atorvastatin treatment in atherosclerotic lesions in apoE/LDLr-deficient mice. Methods: ApoE/LDLr-deficient mice were fed either the western type diet or western type diet enriched by atorvastatin at dose 100 mg/kg per day. Biochemical analysis of blood, immunohistochemical and western blot analysis of endoglin, SMAD2 and eNOS expressions in aorta were performed. Results: Fluorescence immunohistochemistry showed endoglin co-expression with SMAD2 and eNOS in aortic endothelium. Atorvastatin treatment resulted in a strong hypolipidemic effect followed by increase in endoglin serum levels and increase in endothelial expression of endoglin in aortic sinus. Moreover, western blot analysis demonstrated significant increase of endoglin, SMAD2, and eNOS expression in mice aorta after atorvastatin treatment. Conclusion: Based on the results of the study we propose that endoglin might be interesting marker of endothelial dysfunction and/or atherogenesis, which is upregulated by statins implicating potential beneficial role of this molecule and its pathway in atherosclerosis. Funding: This work was supported by grant from The Grant Agency of Charles University in Prague Number 129208/C.
ENDOGLIN EXPRESSION IN ATHEROGENESIS AND AFTER ATORVASTATIN TREATMENT IN APOE/LDLR-DEFICIENT MICE P Nachtigal1, L Vecerova1, S Micuda2, E Brcakova2, D Solichova3 1
Biological and Medical Sciences, Charles University in Prague, Faculty of Pharmacy, Hradec Kralove; 2Pharmacology, Charles University in Prague, Faculty of Medicine, Hradec Kralove; 3 Metabolic Care and Gerontology, Charles University Medical School and Teaching Hospital, Hradec Kralove Objectives: Endoglin (CD 105) has been demonstrated to affect TGF-ȕ signaling and eNOS expression by affecting SMAD2 protein in vitro. Thus, in this study we wanted to elucidate whether endoglin is co-expressed with SMAD2 and eNOS in vivo and whether it is affected by the atorvastatin treatment in atherosclerotic lesions in apoE/LDLr-deficient mice. Methods: ApoE/LDLr-deficient mice were fed either the western type diet or western type diet enriched by atorvastatin at dose 100 mg/kg per day. Biochemical analysis of blood, immunohistochemical and western blot analysis of endoglin, SMAD2 and eNOS expressions in aorta were performed. Results: Fluorescence immunohistochemistry showed endoglin co-expression with SMAD2 and eNOS in aortic endothelium. Atorvastatin treatment resulted in a strong hypolipidemic effect followed by increase in endoglin serum levels and increase in endothelial expression of endoglin in aortic sinus. Moreover, western blot analysis demonstrated significant increase of endoglin, SMAD2, and eNOS expression in mice aorta after atorvastatin treatment. Conclusion: Based on the results of the study we propose that endoglin might be interesting marker of endothelial dysfunction and/or atherogenesis, which is upregulated by statins implicating potential beneficial role of this molecule and its pathway in atherosclerosis. Funding: This work was supported by grant from The Grant Agency of Charles University in Prague Number 129208/C.