ArticleJournal of cellular and molecular medicine2014
Expression of dual nucleotides/cysteinyl-leukotrienes receptor GPR17 in early trafficking of cardiac stromal cells after myocardial infarction.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Computational screening of biomarkers and potential drugs for arthrofibrosis based on combination of sequencing and large nature language model.Journal of orthopaedic translation · 2024Article
- Lung protective effect of Ticagrelor in endotoxemia.Journal of medicine and life · 2023Article
- Mechanistic insight on the role of leukotriene receptors in ischemic-reperfusion injury.Pharmacological reports : PR · 2021Review
- Cangrelor ameliorates CLP-induced pulmonary injury in sepsis by inhibiting GPR17.European journal of medical research · 2021Article
- Gpr17 deficiency in POMC neurons ameliorates the metabolic derangements caused by long-term high-fat diet feeding.Nutrition & diabetes · 2019Article
- GPR17 mediates ischemia-like neuronal injury via microglial activation.International journal of molecular medicine · 2018Article
- Doxorubicin upregulates CXCR4 via miR-200c/ZEB1-dependent mechanism in human cardiac mesenchymal progenitor cells.Cell death & disease · 2017Article
- Role of the Cysteinyl Leukotrienes in the Pathogenesis and Progression of Cardiovascular Diseases.Mediators of inflammation · 2017Review
- Cysteinyl Leukotrienes and Their Receptors: Emerging Therapeutic Targets in Central Nervous System Disorders.CNS neuroscience & therapeutics · 2016Review
- Evaluation of Cysteinyl Leukotriene Signaling as a Therapeutic Target for Colorectal Cancer.Frontiers in cell and developmental biology · 2016Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GPR17 is a G(i) -coupled dual receptor activated by uracil-nucleotides and cysteinyl-leukotrienes. These mediators are massively released into hypoxic tissues. In the normal heart, GPR17 expression has been reported. By contrast, its role in myocardial ischaemia has not yet been assessed. In the present report, the expression of GPR17 was investigated in mice before and at early stages after myocardial infarction by using immunofluorescence, flow cytometry and RT-PCR. Before induction of ischaemia, results indicated the presence of the receptor in a population of stromal cells expressing the stem-cell antigen-1 (Sca-1). At early stages after ligation of the coronary artery, the receptor was expressed in Sca-1(+) cells, and cells stained with Isolectin-B4 and anti-CD45 antibody. GPR17(+) cells also expressed mesenchymal marker CD44. GPR17 function was investigated in vitro in a Sca-1(+)/CD31(-) cell line derived from normal hearts. These experiments showed a migratory function of the receptor by treatment with UDP-glucose and leukotriene LTD4, two GPR17 pharmacological agonists. The GPR17 function was finally assessed in vivo by treating infarcted mice with Cangrelor, a pharmacological receptor antagonist, which, at least in part, inhibited early recruitment of GPR17(+) and CD45(+) cells. These findings suggest a regulation of heart-resident mesenchymal cells and blood-borne cellular species recruitment following myocardial infarction, orchestrated by GPR17.
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