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OBJECTIVE Diabetes mellitus is a major risk factor for cardiovasculardiseases This study explores the role of endoplasmic reticulum ER stressand its link to EGFR activation in microvascular dysfunction and cardiacfibrosis in a -cells depleted and hyperglycemic mice modelRESEARCH DESIGN Endothelium-dependent relaxation EDR and cardiac fibrosiswere assessed in C57BL6J mice receiving STZ 200 mgkg with or withoutepidermal growth factor receptor EGFR inhibitor AG1478 10 mgKgdayER stress inhibitor TUDCA 150 mgKgday or insulin 01 Uday for twoweeksRESULTS ER stress induction in STZ mice was evidenced by an increase ofCHOP ATF4 ATF6 and P-eIF2 expression in heart and mesenteric resistanceartery MRA ER stress markers expression was reduced in STZ mice treatedwith AG1478 TUDCA or insulin We observed a remarkable induction incardiac fibrosis associated with enhanced collagen type-I and PAI-1expression in STZ mice that were reduced with AG1478 TUDCA and insulintreatment Endothelium-dependent relaxation responses expression andphosphorylation of eNOS and endothelium independent sensitivity responseswere decreased in STZ mice compared to control and STZ mice treated withAG1478 TUDCA or insulin The inhibition of eNOS using L-NAME reduced EDRin all groups Additionally NADPH oxidase inhibition with apocyninimproved EDR only in STZ mice The role of NADPH oxidase activity in theendothelium dysfunction was confirmed with the increase of mRNA levels ofNox2 and Nox4 in MRA in STZ mice compared to control and STZ mice treatedwith TUDCA or insulinConclusion These data provide evidence that ER stress induction in type 1diabetes plays a pivotal
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