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Article: N-Propargyl caffeate amide (PACA) prevents cardiac fibrosis in experimental myocardial infarction by promoting pro-resolving macrophage polarization
Title | N-Propargyl caffeate amide (PACA) prevents cardiac fibrosis in experimental myocardial infarction by promoting pro-resolving macrophage polarization |
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Authors | |
Keywords | macrophage polarization cardiac fibrosis N-propargyl caffeate amide PPAR-γ pathway |
Issue Date | 2020 |
Publisher | Impact Journals LLC. The Journal's web site is located at http://www.impactaging.com |
Citation | Aging, 2020, v. 12 n. 6, p. 5384-5398 How to Cite? |
Abstract | Macrophages control the initiation and resolution of cardiac fibrosis in post-infarction cardiac remodeling. The aim of the present study was to investigate whether N-propargyl caffeate amide (PACA) could suppress myocardial fibrosis via regulating macrophage polarization. By using rat model of isoproterenol-induced myocardial fibrosis, we discovered that PACA could reduce cardiac fibrosis in a dose-dependent manner. To elucidate the anti-fibrotic mechanisms, we examined whether PACA affected pro-inflammatory M1 and pro-resolving macrophage biomarkers in macrophage polarization. As result, PACA reduced the expression of pro-inflammatory M1 biomarkers (e.g., iNOS, TNF-α, CXCL10, IL-6, CCL2 and CD80) while increased the expression of pro-resolving M2a biomarkers (e.g., IL-10, arginase-1, FZZ1, YM-1 and CD163) in LPS-stimulated RAW264.7 macrophages. PACA also suppressed the elevation of M1 biomarker ED1 in the early phase but up-regulated the expression of pro-resolving biomarker ED2 in the later phase. Moreover, PACA reduced the expression of pro-fibrotic TGF-β1 and PDGF-α while maintained or even increased the production of pro-apoptotic MMP-13, MMP-9 and TRAIL. Importantly, mechanistic studies revealed that PACA might promote the switch of macrophage polarization towards a pro-resolving macrophage phenotype via activating PPAR-γ pathway. Taken together, this study suggested that PACA might be a drug candidate for preventing cardiac fibrosis in myocardial infarction. |
Persistent Identifier | http://hdl.handle.net/10722/283771 |
ISSN | 2023 Impact Factor: 3.9 2023 SCImago Journal Rankings: 1.180 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | CHENG, Y | - |
dc.contributor.author | LUO, D | - |
dc.contributor.author | ZHAO, Y | - |
dc.contributor.author | Rong, J | - |
dc.date.accessioned | 2020-07-03T08:23:52Z | - |
dc.date.available | 2020-07-03T08:23:52Z | - |
dc.date.issued | 2020 | - |
dc.identifier.citation | Aging, 2020, v. 12 n. 6, p. 5384-5398 | - |
dc.identifier.issn | 1945-4589 | - |
dc.identifier.uri | http://hdl.handle.net/10722/283771 | - |
dc.description.abstract | Macrophages control the initiation and resolution of cardiac fibrosis in post-infarction cardiac remodeling. The aim of the present study was to investigate whether N-propargyl caffeate amide (PACA) could suppress myocardial fibrosis via regulating macrophage polarization. By using rat model of isoproterenol-induced myocardial fibrosis, we discovered that PACA could reduce cardiac fibrosis in a dose-dependent manner. To elucidate the anti-fibrotic mechanisms, we examined whether PACA affected pro-inflammatory M1 and pro-resolving macrophage biomarkers in macrophage polarization. As result, PACA reduced the expression of pro-inflammatory M1 biomarkers (e.g., iNOS, TNF-α, CXCL10, IL-6, CCL2 and CD80) while increased the expression of pro-resolving M2a biomarkers (e.g., IL-10, arginase-1, FZZ1, YM-1 and CD163) in LPS-stimulated RAW264.7 macrophages. PACA also suppressed the elevation of M1 biomarker ED1 in the early phase but up-regulated the expression of pro-resolving biomarker ED2 in the later phase. Moreover, PACA reduced the expression of pro-fibrotic TGF-β1 and PDGF-α while maintained or even increased the production of pro-apoptotic MMP-13, MMP-9 and TRAIL. Importantly, mechanistic studies revealed that PACA might promote the switch of macrophage polarization towards a pro-resolving macrophage phenotype via activating PPAR-γ pathway. Taken together, this study suggested that PACA might be a drug candidate for preventing cardiac fibrosis in myocardial infarction. | - |
dc.language | eng | - |
dc.publisher | Impact Journals LLC. The Journal's web site is located at http://www.impactaging.com | - |
dc.relation.ispartof | Aging | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | macrophage polarization | - |
dc.subject | cardiac fibrosis | - |
dc.subject | N-propargyl caffeate amide | - |
dc.subject | PPAR-γ pathway | - |
dc.title | N-Propargyl caffeate amide (PACA) prevents cardiac fibrosis in experimental myocardial infarction by promoting pro-resolving macrophage polarization | - |
dc.type | Article | - |
dc.identifier.email | Rong, J: jrong@hku.hk | - |
dc.identifier.authority | Rong, J=rp00515 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.18632/aging.102959 | - |
dc.identifier.pmid | 32203054 | - |
dc.identifier.pmcid | PMC7138579 | - |
dc.identifier.scopus | eid_2-s2.0-85083042062 | - |
dc.identifier.hkuros | 310726 | - |
dc.identifier.volume | 12 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 5384 | - |
dc.identifier.epage | 5398 | - |
dc.identifier.isi | WOS:000522733300044 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 1945-4589 | - |