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Conference Paper: ω-Alkynyl arachidonic acid promotes anti-inflammatory M2 polarization of macrophages against acute myocardial infarction via attenuating the expression of iNOS and PKM2
Title | ω-Alkynyl arachidonic acid promotes anti-inflammatory M2 polarization of macrophages against acute myocardial infarction via attenuating the expression of iNOS and PKM2 |
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Authors | |
Issue Date | 2016 |
Publisher | LIPID MAPS |
Citation | LIPID MAPS Annual Meeting 2016: Lipidomics Impact on Metabolic, Cancer, Cardiovascular and Inflammatory Diseases, La Jolla, CA, USA, 17-18 May 2016 How to Cite? |
Abstract | Delayed resolution of inflammation following acute myocardial infarction exacerbates heart injury and impairs cardiac repair. Macrophages exhibit either pro-inflammatory M1 or anti-inflammatory M2 phenotype, and thereby play key roles in acute myocardial infarction. The aim of the present study was to investigate whether ω-alkynyl arachidonic acid could regulate phenotypic and functional switch of macrophages in myocardial infarction. We initially discovered that ω-alkynyl arachidonic acid selectively suppressed the up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated macrophages. We also found that ω-alkynyl arachidonic acid not only reduced the expression of M1 markers (TNF-α, CXCL10, iNOS and IL-6) but also increased the expression of M2 markers (IL-10 and arginase I) in LPS-stimulated macrophages. Moreover, ω-alkynyl arachidonic acid markedly enhanced the phagocytosis of fluorescently-labeled beads or apoptotic H9c2 cardiac cells. These results stimulated us to further investigate the cardioprotective activities of ω-alkynyl
arachidonic acid in a mouse model of myocardial infarction. ω-Alkynyl arachidonic acid indeed reduced infarct size, cardiac damage and the release of myocardial enzymes CK-MB. To elucidate the underlying mechanisms, we intended to identify the covalent ω-alkynyl arachidonic acid-protein adducts. By performing biotinylation to the cellular proteins via “click chemistry” alkyne-azido cycloaddition, we isolated glycolytic enzyme pyruvate kinase M2 (PKM2) as a predominant ω-alkynyl arachidonic acid binding protein. ω-Alkynyl arachidonic acid could also attenuate PKM2 expression and suppress nuclear translocation of PKM2 in LPS-stimulated macrophages. Thus, ω-alkynyl arachidonic acid may promote anti-inflammatory M2 polarization of macrophages against acute myocardial infarction via regulating the expression of PKM2 and iNOS. |
Persistent Identifier | http://hdl.handle.net/10722/246399 |
DC Field | Value | Language |
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dc.contributor.author | Cheng, Y | - |
dc.contributor.author | Rong, J | - |
dc.date.accessioned | 2017-09-18T02:27:50Z | - |
dc.date.available | 2017-09-18T02:27:50Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | LIPID MAPS Annual Meeting 2016: Lipidomics Impact on Metabolic, Cancer, Cardiovascular and Inflammatory Diseases, La Jolla, CA, USA, 17-18 May 2016 | - |
dc.identifier.uri | http://hdl.handle.net/10722/246399 | - |
dc.description.abstract | Delayed resolution of inflammation following acute myocardial infarction exacerbates heart injury and impairs cardiac repair. Macrophages exhibit either pro-inflammatory M1 or anti-inflammatory M2 phenotype, and thereby play key roles in acute myocardial infarction. The aim of the present study was to investigate whether ω-alkynyl arachidonic acid could regulate phenotypic and functional switch of macrophages in myocardial infarction. We initially discovered that ω-alkynyl arachidonic acid selectively suppressed the up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated macrophages. We also found that ω-alkynyl arachidonic acid not only reduced the expression of M1 markers (TNF-α, CXCL10, iNOS and IL-6) but also increased the expression of M2 markers (IL-10 and arginase I) in LPS-stimulated macrophages. Moreover, ω-alkynyl arachidonic acid markedly enhanced the phagocytosis of fluorescently-labeled beads or apoptotic H9c2 cardiac cells. These results stimulated us to further investigate the cardioprotective activities of ω-alkynyl arachidonic acid in a mouse model of myocardial infarction. ω-Alkynyl arachidonic acid indeed reduced infarct size, cardiac damage and the release of myocardial enzymes CK-MB. To elucidate the underlying mechanisms, we intended to identify the covalent ω-alkynyl arachidonic acid-protein adducts. By performing biotinylation to the cellular proteins via “click chemistry” alkyne-azido cycloaddition, we isolated glycolytic enzyme pyruvate kinase M2 (PKM2) as a predominant ω-alkynyl arachidonic acid binding protein. ω-Alkynyl arachidonic acid could also attenuate PKM2 expression and suppress nuclear translocation of PKM2 in LPS-stimulated macrophages. Thus, ω-alkynyl arachidonic acid may promote anti-inflammatory M2 polarization of macrophages against acute myocardial infarction via regulating the expression of PKM2 and iNOS. | - |
dc.language | eng | - |
dc.publisher | LIPID MAPS | - |
dc.relation.ispartof | LIPID MAPS Annual Meeting 2016 | - |
dc.title | ω-Alkynyl arachidonic acid promotes anti-inflammatory M2 polarization of macrophages against acute myocardial infarction via attenuating the expression of iNOS and PKM2 | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Rong, J: jrong@hku.hk | - |
dc.identifier.authority | Rong, J=rp00515 | - |
dc.identifier.hkuros | 276387 | - |
dc.publisher.place | United States | - |