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论文题目: Endogenously Generated Omega-3 Fatty Acids Attenuate Vascular Inflammation and Neointimal Hyperplasia by Interaction With Free Fatty Acid Receptor 4 in Mice
英文论文题目: Endogenously Generated Omega-3 Fatty Acids Attenuate Vascular Inflammation and Neointimal Hyperplasia by Interaction With Free Fatty Acid Receptor 4 in Mice
第一作者: Li, XZ; Ballantyne, LL; Che, XH; Mewburn, JD; Kang, JX; Barkley, RM; Murphy, RC; Yu, Y; Funk, CD
英文第一作者: Li, XZ; Ballantyne, LL; Che, XH; Mewburn, JD; Kang, JX; Barkley, RM; Murphy, RC; Yu, Y; Funk, CD
联系作者: Funk, CD (reprint author), Queens Univ, Dept Biomed & Mol Sci, Botterell Hall,Room 433,18 Stuart St, Kingston, ON K7L 3N6, Canada.
英文联系作者: Funk, CD (reprint author), Queens Univ, Dept Biomed & Mol Sci, Botterell Hall,Room 433,18 Stuart St, Kingston, ON K7L 3N6, Canada.
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发表年度: 2015
卷: 4
期: 4
页码: -
摘要: Background-Omega-3 polyunsaturated fatty acids (omega 3 PUFAs) suppress inflammation through activation of free fatty acid receptor 4 (FFAR4), but this pathway has not been explored in the context of cardiovascular disease. We aimed to elucidate the involvement of FFAR4 activation by omega 3 PUFAs in the process of vascular inflammation and neointimal hyperplasia in mice. Methods and Results-We used mice with disruption of FFAR4 (Ffar4(-/-)), along with a strain that synthesizes high levels of omega 3 PUFAs (fat-1) and a group of crossed mice (Ffar4(-/-)/fat-1), to elucidate the role of FFAR4 in vascular dysfunction using acute and chronic thrombosis/vascular remodeling models. The presence of FFAR4 in vascular-associated cells including perivascular adipocytes and macrophages, but not platelets, was demonstrated. omega 3 PUFAs endogenously generated in fat-1 mice (n=9), but not in compound Ffar4(-/-)/fat-1 mice (n=9), attenuated femoral arterial thrombosis induced by FeCl3. Neointimal hyperplasia and vascular inflammation in the common carotid artery were significantly curtailed 4 weeks after FeCl3 injury in fat-1 mice (n=6). This included greater luminal diameter and enhanced blood flow, reduced intima: media ratio, and diminished macrophage infiltration in the vasculature and perivascular adipose tissue compared with control mice. These effects were attenuated in the Ffar4(-/-)/fat-1 mice. Conclusions-These results indicate that omega 3 PUFAs mitigate vascular inflammation, arterial thrombus formation, and neointimal hyperplasia by interaction with FFAR4 in mice. Moreover, the omega 3 PUFA-FFAR4 pathway decreases inflammatory responses with dampened macrophage transmigration and infiltration.
英文摘要: Background-Omega-3 polyunsaturated fatty acids (omega 3 PUFAs) suppress inflammation through activation of free fatty acid receptor 4 (FFAR4), but this pathway has not been explored in the context of cardiovascular disease. We aimed to elucidate the involvement of FFAR4 activation by omega 3 PUFAs in the process of vascular inflammation and neointimal hyperplasia in mice. Methods and Results-We used mice with disruption of FFAR4 (Ffar4(-/-)), along with a strain that synthesizes high levels of omega 3 PUFAs (fat-1) and a group of crossed mice (Ffar4(-/-)/fat-1), to elucidate the role of FFAR4 in vascular dysfunction using acute and chronic thrombosis/vascular remodeling models. The presence of FFAR4 in vascular-associated cells including perivascular adipocytes and macrophages, but not platelets, was demonstrated. omega 3 PUFAs endogenously generated in fat-1 mice (n=9), but not in compound Ffar4(-/-)/fat-1 mice (n=9), attenuated femoral arterial thrombosis induced by FeCl3. Neointimal hyperplasia and vascular inflammation in the common carotid artery were significantly curtailed 4 weeks after FeCl3 injury in fat-1 mice (n=6). This included greater luminal diameter and enhanced blood flow, reduced intima: media ratio, and diminished macrophage infiltration in the vasculature and perivascular adipose tissue compared with control mice. These effects were attenuated in the Ffar4(-/-)/fat-1 mice. Conclusions-These results indicate that omega 3 PUFAs mitigate vascular inflammation, arterial thrombus formation, and neointimal hyperplasia by interaction with FFAR4 in mice. Moreover, the omega 3 PUFA-FFAR4 pathway decreases inflammatory responses with dampened macrophage transmigration and infiltration.
刊物名称: JOURNAL OF THE AMERICAN HEART ASSOCIATION
英文刊物名称: JOURNAL OF THE AMERICAN HEART ASSOCIATION
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学科: Cardiovascular System & Cardiology
英文学科: Cardiovascular System & Cardiology
影响因子: 4.306
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论文类别: Article
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