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• W4386871683 abstract "Abstract Rationale and purpose Prevention or attenuation of heart failure (HF) is persistent task in clinic as well as challenge for progress in research. Both, intercellular connexin-43 (Cx43) channels and extracellular matrix (ECM) exert high impact on heart function. Thus, we aimed to explore whether HF due to volume overload (VO) induces alterations in myocardial Cx43, ECM proteins MMP2, SMAD2/3, TGFβ1 and PKC signaling as well as changes that may be revealed by enzyme histochemistry. Moreover, we tested the impact of treatment suppressing RAS on examined targeted proteins. Methods VO-HF was induced in male normotensive Hannover Sprague- Dawley (HSD) and mRen-2 transgenic hypertensive (TGR) rats by creating an aorto-caval fistula (ACF) and heart response was examined 20-weeks later. Sham-rats were compared with non-treated rats with ACF and those treated for 15-weeks with ACEI (trandolapril, 6mg/l, p.o.) or ARB (losartan (200mg/l, p.o.). Left ventricular heart (LV) tissue was analyzed using western blot, zymography and enzyme histochemistry. Key results Echocardiography confirmed an increase in cardiac output and a decrease in ejection fraction in both strains of rats. BW was higher in TGR vs HSD and it was not affected by VO. HW and LVW were higher in TGR vs HSD and VO increased both parameters regardless the strain while ACEI&gt;ARB attenuated it. In parallel, myocardial pro-hypertrophic PKCd expression was higher in TGR vs HSD and increased in both strains due to VO while both drugs prevent it. Glycogen phosphorylase and capillary associated 5-nucleotidase, alkaline phospatase and dipeptidyl peptidase IV activities were reduced due to VO in HSD and TGR and it was attenuated by treatment. Cx43 expression and its functional phosphorylation status were lower in TGR vs HSD and suppressed in both strains due to VO but ACEI&gt;ARB prevented it. Similar trend of changes was observed in PKCe expression, which phosphorylates Cx43. Profibrotic TGFβ1-Smad2/3 pathway was suppressed along with reduced MMP2 activity in TGR comparing to HSD. VO reduced SMAD2/3 in HSD and TGFβ1 in TGR as well as MMP2 expression in both strains, whereby treatment abolished these changes. VO decreased MMP2 (63kDa) activity only in TGR and ARB prevented it. VO did not affect collagen deposition in either strain vs sham rats. Conclusions Hypertrophic and hypofibrotic phenotypes are induced by volume overload in both rat strains. Together with deterioration of Cx43 mediated intercellular coupling it may contribute to heart dysfunction. Inhibition of RAS components attenuates progression of VO and its adverse consequences. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic VEGA 2/0158/19, 2/0002/20" @default.
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• W4386871683 date "2021-10-01" @default.
• W4386871683 modified "2023-09-27" @default.
• W4386871683 title "Inhibition of RAS components attenuates progression of heart failure and its adverse consequences on myocardial remodeling in both normotensive and hypertensive rats" @default.
• W4386871683 doi "https://doi.org/10.1093/eurheartj/ehab724.3185" @default.
• W4386871683 hasPublicationYear "2021" @default.
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