| http://purl.uniprot.org/citations/19358330 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19358330 | http://www.w3.org/2000/01/rdf-schema#comment | "Fibroblast growth factor receptor (FGFR) is expressed in a variety of cells and is involved in their proliferation/migration/survival. To elucidate FGFR-mediated specific action of vascular endothelial cells (ECs) on myocardial ischemia, we generated endothelium-targeted transgenic mice overexpressing constitutively active FGFR2 using Tie2 promoter (FGFR2-Tg). Infarct size, vessel formation and blood perfusion were significantly improved 28 days after myocardial infarction (MI) in FGFR2-Tg, compared with wild-type mice. Aortic ECs isolated from FGFR-Tg showed a marked increase in migratory capacity and tube formation. These in vitro angiogenic activities were blocked by PI3-kinase inhibitor. Whereas, parameters obtained from echocardiography were already improved at three days after MI. Cardiomyocyte apoptosis at the ischemic border zone was decreased in FGFR2-Tg (32.1%, p < 0.05) and cardiac mRNA expression of FGF2 (basic FGF) was also up-regulated (142%, p < 0.05) at 3 days after MI. 1% oxygen-mediated apoptosis was significantly inhibited in FGFR2-Tg-ECs and this inhibition was abolished by PI3-kinase inhibitor. FGFR2-Tg-ECs exposed to 1% oxygen exhibited enhanced phosphorylation of 416-Tyr-Src, 473-Ser-Akt, and HIF1alpha accumulation. The production of FGF2 was enhanced 2.1-fold in FGFR-Tg-ECs under 1% oxygen via the Src/Akt/HIF1alpha pathway, which induced the peri-vessel migration of vascular smooth muscle cells (VSMCs) and anti-apoptotic effects on VSMCs and cardiomyocytes. FGF receptor signaling in ECs promoted migration, survival and autocrine production of FGF2, leading to reduced infarct size, which is associated with anti-apoptotic action in the early stage and with enhanced angiogenesis in the late stage after MI."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yjmcc.2009.01.015"xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Matsunaga S."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Matsubara H."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Kurihara T."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Takeda M."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Matoba Y."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Adachi Y."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Matoba S."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Matsui A."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Tatsumi T."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Katsume A."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Okigaki M."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Mansukhani A."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Che J."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Kobara M."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Honsho S."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Jishan C."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/author | "Kishita E."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/name | "J Mol Cell Cardiol"xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/pages | "663-673"xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/title | "Endothelium-targeted overexpression of constitutively active FGF receptor induces cardioprotection in mice myocardial infarction."xsd:string |
| http://purl.uniprot.org/citations/19358330 | http://purl.uniprot.org/core/volume | "46"xsd:string |