| http://purl.uniprot.org/citations/26739490 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26739490 | http://www.w3.org/2000/01/rdf-schema#comment | "We have demonstrated that glucagon like peptide-1 (GLP-1) protects the heart against ischemic injury. However, the physiological mechanism by which GLP-1 receptor (GLP-1R) initiates cardioprotection remains to be determined. The objective of this study is to elucidate the functional roles of MAPK kinase 3 (MKK3) and Akt-1 in mediating exendin-4-elicited protection in the infarcted hearts. Adult mouse myocardial infarction (MI) was created by ligation of the left descending artery. Wild-type, MKK3(-/-), Akt-1(-/-), and Akt-1(-/-);MKK3(-/-) mice were divided into one of several groups: 1) sham: animals underwent thoracotomy without ligation; 2) MI: animals underwent MI and received a daily dose of intraperitoneal injection of vehicle (saline); 3) MI + exendin-4: infarcted mice received daily injections of exendin-4, a GLP-1R agonist (0.1 mg/kg, ip). Echocardiographic measurements indicate that exendin-4 treatment resulted in the preservation of ventricular function and increases in the survival rate, but these effects were diminished in MKK3(-/-), Akt-1(-/-), and Akt-1(-/-);MKK3(-/-) mice. Exendin-4 treatments suppressed cardiac hypotrophy and reduced scar size and cardiac interstitial fibrosis, respectively, but these beneficial effects were lost in genetic elimination of MKK3, Akt-1, or Akt-1(-/-);MKK3(-/-) mice. GLP-1R stimulation stimulated angiogenic responses, which were also mitigated by deletion of MKK3 and Akt-1. Exendin-4 treatment increased phosphorylation of MKK3, p38, and Akt-1 at Ser129 but decreased levels of active caspase-3 and cleaved poly (ADP-ribose) polymerase; these proteins were diminished in MKK3(-/-), Akt-1(-/-), and Akt-1(-/-);MKK3(-/-) mice. These results reveal that exendin-4 treatment improves cardiac function, attenuates cardiac remodeling, and promotes angiogenesis in the infarcted myocardium through MKK3 and Akt-1 pathway."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpcell.00194.2015"xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Du J."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Wang Z."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Wei L."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Zhuang S."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Qin G."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Zhao T.C."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Yano N."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Zhao Y.T."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Liu P.Y."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/author | "Dubielecka-Szczerba P."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/name | "Am J Physiol Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/pages | "C270-83"xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/title | "Exendin-4 induces myocardial protection through MKK3 and Akt-1 in infarcted hearts."xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://purl.uniprot.org/core/volume | "310"xsd:string |
| http://purl.uniprot.org/citations/26739490 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26739490 |
| http://purl.uniprot.org/citations/26739490 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/26739490 |
| http://purl.uniprot.org/uniprot/#_D3Z783-mappedCitation-26739490 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26739490 |
| http://purl.uniprot.org/uniprot/#_D3YYP9-mappedCitation-26739490 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26739490 |
| http://purl.uniprot.org/uniprot/#_D3YXX3-mappedCitation-26739490 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26739490 |
| http://purl.uniprot.org/uniprot/#_A0A0R4J1Q6-mappedCitation-26739490 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26739490 |