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2 results on '"omega‐3 fatty acid receptor"'

1. Endogenously Generated Omega‐3 Fatty Acids Attenuate Vascular Inflammation and Neointimal Hyperplasia by Interaction With Free Fatty Acid Receptor 4 in Mice

Author

Robert C. Murphy, Xinghui Che, Colin D. Funk, Jeffrey Mewburn, Laurel L. Ballantyne, Ying Yu, Jing X. Kang, Robert M. Barkley, and Xinzhi Li

Subjects
Vasculitis, medicine.medical_specialty, Carotid Artery, Common, Fluorescent Antibody Technique, Adipose tissue, Inflammation, Context (language use), Vascular Medicine, fatty acids, Receptors, G-Protein-Coupled, Mice, Internal medicine, Fatty Acids, Omega-3, medicine, Animals, Platelet, Original Research, Mice, Knockout, Neointimal hyperplasia, chemistry.chemical_classification, Hyperplasia, Reverse Transcriptase Polymerase Chain Reaction, business.industry, medicine.disease, Tunica intima, adipose tissue, omega‐3 fatty acid receptor, Femoral Artery, Mice, Inbred C57BL, Endocrinology, medicine.anatomical_structure, chemistry, transgenic model, Immunology, medicine.symptom, Tunica Intima, Cardiology and Cardiovascular Medicine, business, Polyunsaturated fatty acid
Abstract

Background Omega‐3 polyunsaturated fatty acids (ω3 PUFA s) suppress inflammation through activation of free fatty acid receptor 4 ( FFAR 4), but this pathway has not been explored in the context of cardiovascular disease. We aimed to elucidate the involvement of FFAR 4 activation by ω3 PUFA s in the process of vascular inflammation and neointimal hyperplasia in mice. Methods and Results We used mice with disruption of FFAR 4 ( Ffar4 −/− ), along with a strain that synthesizes high levels of ω3 PUFA s ( fat‐1 ) and a group of crossed mice ( Ffar4 −/− / fat‐1 ), to elucidate the role of FFAR 4 in vascular dysfunction using acute and chronic thrombosis/vascular remodeling models. The presence of FFAR 4 in vascular‐associated cells including perivascular adipocytes and macrophages, but not platelets, was demonstrated. ω3 PUFA s endogenously generated in fat‐1 mice (n=9), but not in compound Ffar4 −/− / fat‐1 mice (n=9), attenuated femoral arterial thrombosis induced by FeCl 3 . Neointimal hyperplasia and vascular inflammation in the common carotid artery were significantly curtailed 4 weeks after FeCl 3 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 ω3 PUFA s mitigate vascular inflammation, arterial thrombus formation, and neointimal hyperplasia by interaction with FFAR 4 in mice. Moreover, the ω3 PUFA – FFAR 4 pathway decreases inflammatory responses with dampened macrophage transmigration and infiltration.

Published
2015
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2. Endogenously generated omega-3 fatty acids attenuate vascular inflammation and neointimal hyperplasia by interaction with free fatty acid receptor 4 in mice.

Author

Li X, Ballantyne LL, Che X, Mewburn JD, Kang JX, Barkley RM, Murphy RC, Yu Y, and Funk CD

Subjects
Animals, Carotid Artery, Common pathology, Carotid Artery, Common physiopathology, Femoral Artery pathology, Femoral Artery physiopathology, Fluorescent Antibody Technique, Hyperplasia, Inflammation metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, G-Protein-Coupled metabolism, Reverse Transcriptase Polymerase Chain Reaction, Tunica Intima physiopathology, Vasculitis metabolism, Vasculitis physiopathology, Fatty Acids, Omega-3 physiology, Inflammation physiopathology, Receptors, G-Protein-Coupled physiology, Tunica Intima pathology
Abstract

Background: Omega-3 polyunsaturated fatty acids (ω3 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 ω3 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 ω3 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. ω3 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 ω3 PUFAs mitigate vascular inflammation, arterial thrombus formation, and neointimal hyperplasia by interaction with FFAR4 in mice. Moreover, the ω3 PUFA-FFAR4 pathway decreases inflammatory responses with dampened macrophage transmigration and infiltration., (© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Published
2015
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