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http://purl.uniprot.org/citations/26739213http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26739213http://www.w3.org/2000/01/rdf-schema#comment"

Aims

Dipeptidyl peptidase-4 (DPP-4) inhibitors are reported to have protective effects on various cells but it is unclear how DPP-4 inhibitors have cardioprotective effects. Our aim was to study the mechanisms of cardioprotective effects by DPP-4 inhibition.

Methods and results

C57BL/6 mice and DPP-4 knockout (DPP-4KO) mice were subjected to left coronary artery ligation to produce acute myocardial infarction (MI). C57BL/6 mice were then treated with vehicle or DPP-4 inhibitor. Left ventricular function, infarct size, the number of vessels, and myocardial ischemia were assessed at 5days after MI. The treatment with DPP-4 inhibitor significantly improved cardiac function and decreased the infarct size. DPP-4 inhibitor increased the ratio of endothelial cell numbers to a cardiomyocyte. The extent of myocardial ischemia and the number of TUNEL-positive cells in the border area were significantly decreased by DPP-4 inhibitor. Stromal cell-derived factor-1α (SDF-1α) level in myocardium was significantly increased by DPP-4 inhibitor. Those cardioprotective effects after MI were also recognized in DPP-4KO mice. DPP-4 protein was expressed on rat neonatal cardiomyocytes and DPP-4 inhibitor significantly reduced hypoxia-induced apoptosis in the cardiomyocytes. However, this effect was abolished by the pretreatment with a CXCR4 antagonist or a signal transducer and activator of transcription 3 (STAT3) inhibitor. The beneficial effects of DPP-4 inhibitor on heart failure after MI were abolished by cardiomyocyte-specific deletion of STAT3.

Conclusions

DPP-4 inhibition may have direct protective effects on the post-MI heart by inducing an antiapoptotic effect and inhibiting a decrease in vessel number through the SDF-1α/CXCR4-mediated STAT3 signaling pathway."xsd:string
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http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Kobayashi Y."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Hirose M."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Takano H."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Hasegawa H."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Kubota A."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Komuro I."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Yamada-Inagawa T."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Kobara Y."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/author"Tadokoro H."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/name"J Mol Cell Cardiol"xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/pages"72-80"xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/title"DPP-4 inhibition has beneficial effects on the heart after myocardial infarction."xsd:string
http://purl.uniprot.org/citations/26739213http://purl.uniprot.org/core/volume"91"xsd:string
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