http://purl.uniprot.org/citations/29287725 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/29287725 | http://www.w3.org/2000/01/rdf-schema#comment | "We found that the anticoagulant plasma protease, activated protein C (APC), stimulates the energy sensor kinase, AMPK, in the stressed heart by activating protease-activated receptor 1 (PAR1) on cardiomyocytes. Wild-type (WT) and AMPK-kinase dead (KD) transgenic mice were subjected to transverse aortic constriction (TAC) surgery. The results demonstrated that while no phenotypic differences can be observed between WT and AMPK-KD mice under normal physiological conditions, AMPK-KD mice exhibit significantly larger hearts after 4 weeks of TAC surgery. Analysis by echocardiography suggested that the impairment in the cardiac function of AMPK-KD hearts is significantly greater than that of WT hearts. Immunohistochemical staining revealed increased macrophage infiltration and ROS generation in AMPK-KD hearts after 4 weeks of TAC surgery. Immunoblotting results demonstrated that the redox markers, pShc66, 4-hydroxynonenal and ERK, were all up-regulated at a higher extent in AMPK-KD hearts after 4 weeks of TAC surgery. Administration of APC-WT and the signaling selective APC-2Cys mutant, but not the anticoagulant selective APC-E170A mutant, significantly attenuated pressure overload-induced hypertrophy and fibrosis. Macrophage infiltration and pShc66 activation caused by pressure overload were also inhibited by APC and APC-2Cys but not by APC-E170A. Therefore, the cardiac AMPK protects against pressure overload-induced hypertrophy and the signaling selective APC-2Cys may have therapeutic potential for treating hypertension-related hypertrophy without increasing the risk of bleeding."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2017.12.125"xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Yang L."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Quan N."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Rezaie A.R."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Cates C."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/author | "Rousselle T."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/pages | "2584-2594"xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/title | "Activated protein C protects against pressure overload-induced hypertrophy through AMPK signaling."xsd:string |
http://purl.uniprot.org/citations/29287725 | http://purl.uniprot.org/core/volume | "495"xsd:string |
http://purl.uniprot.org/citations/29287725 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29287725 |
http://purl.uniprot.org/citations/29287725 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29287725 |
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http://purl.uniprot.org/uniprot/Q8BRK8 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29287725 |
http://purl.uniprot.org/uniprot/G8XUU5 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29287725 |