Proteomic and transcriptomic analysis of heart failure due to volume overload in a rat aortocaval fistula model provides support for new potential therapeutic targets - monoamine oxidase A and transglutaminase 2

0372265 - ÚMG 2012 RIV GB eng J - Článek v odborném periodiku
Petrák, J. - Pospíšilová, J. - Šedinová, M. - Jedelský, P. - Lorková, L. - Vít, O. - Kolář, Michal - Strnad, Hynek - Beneš, J. - Sedmera, David - Červenka, L. - Melenovský, V.
Proteomic and transcriptomic analysis of heart failure due to volume overload in a rat aortocaval fistula model provides support for new potential therapeutic targets - monoamine oxidase A and transglutaminase 2.
Proteome Science. Roč. 9, č. 1 (2011), e69. E-ISSN 1477-5956
Grant CEP: GA MŠMT(CZ) 1M0510
Výzkumný záměr: CEZ:AV0Z50110509; CEZ:AV0Z50520514
Klíčová slova: heart failure * monoamine oxidase A * transglutaminase 2
Kód oboru RIV: EB - Genetika a molekulární biologie
Impakt faktor: 2.328, rok: 2011

Chronic hemodynamic overloading leads to heart failure (HF) due to incompletely understood mechanisms. To gain deeper insight into the molecular pathophysiology of volume overload-induced HF and to identify potential markers and targets for novel therapies, we performed proteomic and mRNA expression analysis comparing myocardium from Wistar rats with HF induced by chronic aorto-caval fistula (ACF) and sham-operated rats harvested at the advanced, decompensated stage of HF. In the proteomic analysis we identified 2030 myocardial proteins, of which 66 proteins were differentially expressed. The mRNA expression analysis identified 851 differentially expressed mRNAs. The differentially expressed proteins confirm a switch in the substrate preference from fatty acids to other sources in the failing heart. Among the most upregulated proteins in ACF hearts were monoamine oxidase A and transglutaminase 2 which are both potential targets of low molecular weight inhibitors in future HF therapy.
Trvalý link: http://hdl.handle.net/11104/0205621