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Article ; Online: Insights into the role of the resolvin D2-GPR18 signaling axis in cardiovascular physiology and disease.

Spite, Matthew / Fredman, Gabrielle

Advances in pharmacology (San Diego, Calif.)

2023 Volume 97, Page(s) 257–281

Abstract: Non-resolving inflammation is an underpinning of cardiovascular diseases including atherosclerosis. The resolution of inflammation is an active and highly coordinated process that involves the generation of specialized pro-resolving mediators (SPMs), and ...

Abstract	Non-resolving inflammation is an underpinning of cardiovascular diseases including atherosclerosis. The resolution of inflammation is an active and highly coordinated process that involves the generation of specialized pro-resolving mediators (SPMs), and other factors including proteins, gases, and nucleotides. SPMs comprise a superfamily of lipid mediators that includes lipoxins, resolvins, maresins and protectins. SPMs act through distinct G protein-coupled receptors (GPCRs) and have been extensively studied in animal models of cardiovascular diseases. An emerging body of literature suggests that SPMs have protective roles in atherosclerosis as demonstrated using specific SPM as well as mice deficient in their receptors. This review will highlight a relatively new pro-resolving signaling axis, namely Resolvin D2-GPR18, and how understanding detailed mechanisms and cellular specificity of this signaling axis may help inform the development of more targeted pro-resolution therapies for atherosclerosis and related cardiovascular pathologies.
MeSH term(s)	Humans ; Mice ; Animals ; Cardiovascular Diseases/drug therapy ; Inflammation Mediators/metabolism ; Inflammation/metabolism ; Atherosclerosis/drug therapy ; Cardiovascular Physiological Phenomena ; Receptors, G-Protein-Coupled
Chemical Substances	resolvin D2 ; Inflammation Mediators ; GPR18 protein, human ; Receptors, G-Protein-Coupled ; GPR18 protein, mouse
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural
ISSN	1557-8925
ISSN (online)	1557-8925
DOI	10.1016/bs.apha.2022.12.005
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Article ; Online: Resolving inflammation in nonalcoholic steatohepatitis.

Spite, Matthew

The Journal of clinical investigation

2019 Volume 129, Issue 4, Page(s) 1524–1526

Abstract: Chronic unresolved inflammation contributes to the development of nonalcoholic steatohepatitis (NASH), a disorder characterized by lipotoxicity, fibrosis, and progressive liver dysfunction. In this issue of the JCI, Han et al. report that maresin 1 (MaR1) ...

Abstract	Chronic unresolved inflammation contributes to the development of nonalcoholic steatohepatitis (NASH), a disorder characterized by lipotoxicity, fibrosis, and progressive liver dysfunction. In this issue of the JCI, Han et al. report that maresin 1 (MaR1), a proresolving lipid mediator, mitigates NASH by reprograming macrophages to an antiinflammatory phenotype. Mechanistically, they identified retinoic acid-related orphan receptor α (RORα) as both a target and autocrine regulator of MaR1 production. Because NASH is associated with many widely occurring metabolic diseases, including obesity and type 2 diabetes, identification of this endogenous protective pathway could have broad therapeutic implications.
MeSH term(s)	Arachidonate 12-Lipoxygenase ; Diabetes Mellitus, Type 2 ; Docosahexaenoic Acids ; Humans ; Inflammation ; Non-alcoholic Fatty Liver Disease
Chemical Substances	7,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acid ; Docosahexaenoic Acids (25167-62-8) ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31)
Language	English
Publishing date	2019-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI127583
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Article ; Online: Proresolving receptor tames inflammation in atherosclerosis.

Mena, Hebe Agustina / Spite, Matthew

The Journal of clinical investigation

2021 Volume 131, Issue 24

Abstract: Nonresolving inflammation contributes to the progression of atherosclerosis, a chronic disease characterized by the accumulation of lipid-rich arterial plaques infiltrated with immune cells. In this issue of the JCI, Arnardottir and Thul et al. report ... ...

Abstract	Nonresolving inflammation contributes to the progression of atherosclerosis, a chronic disease characterized by the accumulation of lipid-rich arterial plaques infiltrated with immune cells. In this issue of the JCI, Arnardottir and Thul et al. report that GPR32, a receptor for proresolving lipid mediators including resolvin D1, was decreased in human atherosclerotic lesions and that overexpression of this human receptor in mice reduced lesion area and necrosis of atherosclerotic plaques. Mechanistically, GPR32 signaling blunted the production of proinflammatory cytokines, enhanced macrophage phagocytosis, and reduced leukocyte accumulation. These results suggest that therapeutic targeting of GPR32 could be an approach to resolving chronic inflammation in atherosclerosis.
MeSH term(s)	Animals ; Atherosclerosis/drug therapy ; Atherosclerosis/genetics ; Inflammation/drug therapy ; Macrophages ; Mice ; Phagocytosis ; Plaque, Atherosclerotic
Language	English
Publishing date	2021-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI155240
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Article ; Online: Resolving lipids: lipoxins regulate reverse cholesterol transport.

Spite, Matthew

Cell metabolism

2014 Volume 20, Issue 6, Page(s) 935–937

Abstract: Disruptions in cholesterol homeostasis contribute to cardiovascular disease (CVD). In a recent issue of Cell Metabolism, Demetz et al. (2014) report that endogenous lipoxygenase-mediated metabolism of another lipid, arachidonic acid, produces lipoxins ... ...

Abstract	Disruptions in cholesterol homeostasis contribute to cardiovascular disease (CVD). In a recent issue of Cell Metabolism, Demetz et al. (2014) report that endogenous lipoxygenase-mediated metabolism of another lipid, arachidonic acid, produces lipoxins that regulate reverse cholesterol transport. These results suggest that lipoxins may represent a novel class of therapeutics for CVD.
MeSH term(s)	Animals ; Arachidonic Acid/metabolism ; Cholesterol/metabolism ; Humans ; Metabolome
Chemical Substances	Arachidonic Acid (27YG812J1I) ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2014-12-02
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2014.11.012
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Article ; Online: Brown adipose tissue activation in humans increases plasma levels of lipid mediators.

Walker, Mary E / Kodani, Sean D / Mena, Hebe Agustina / Tseng, Yu-Hua / Cypess, Aaron M / Spite, Matthew

The Journal of clinical endocrinology and metabolism

2024

Abstract: Context: Activation of brown adipose tissue (BAT) thermogenesis improves insulin sensitivity and is beneficial in obesity. Emerging evidence indicates that BAT activation increases lipid mediators that play autocrine and endocrine roles to regulate ... ...

Abstract	Context: Activation of brown adipose tissue (BAT) thermogenesis improves insulin sensitivity and is beneficial in obesity. Emerging evidence indicates that BAT activation increases lipid mediators that play autocrine and endocrine roles to regulate metabolism and inflammation. Objective: The goal of the study was to determine the relationship between two distinct approaches of BAT activation (cold exposure and mirabegron treatment) with lipid mediators in humans. Methods: Healthy female subjects (n = 14) were treated with β3-adrenergic receptor agonist mirabegron (100 mg) daily for 28 days. A subset of female subjects (n = 8) was additionally exposed to cold temperatures (14-16°C) for 2 hours using a cooling vest prior to initiating mirabegron treatment. Main outcome measures: A panel of lipid mediators was assessed in plasma using targeted liquid chromatography-tandem mass spectrometry, and their relationship to anthropometric and metabolic parameters was determined. Results: Activation of BAT with cold exposure acutely increased levels of lipoxygenase and cyclooxygenase products, including 12-hydroxyeicosapentaenoic acid (HEPE), 12-hydroxyeicosatetraenoic acid (HETE), 5-HETE, 14-hydroxydocosahexaenoic acid (HDHA), an isomer of maresin 2 (MaR2), 17-HDHA, protectin D1 (PD1), and prostaglandin E2 (PGE2). Mirabegron treatment similarly increased these products acutely, although levels of some mediators were blunted after chronic mirabegron treatment. Selected lipid mediators, including a MaR2 isomer, 17-HDHA, 5-HETE, and 15-HETE, positively correlated with non-esterified fatty acids and negatively correlated with the respiratory quotient, while PD1, 15-HETE, and 5-HETE positively correlated with adiponectin. Conclusion: These results indicate that selected lipid mediators may serve as biomarkers of BAT activation.
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgae016
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Article ; Online: Resolvin D2 limits atherosclerosis progression via myeloid cell-GPR18.

Lipscomb, Masharh / Walis, Sean / Marinello, Michael / Mena, Hebe Agustina / MacNamara, Katherine C / Spite, Matthew / Fredman, Gabrielle

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2024 Volume 38, Issue 6, Page(s) e23555

Abstract: Dysregulated inflammation-resolution programs are associated with atherosclerosis progression. Resolvins, in part, mediate inflammation-resolution programs. Indeed, Resolvin D2 (RvD2) activates GPR18, a G-protein-coupled receptor, and limits plaque ... ...

Abstract	Dysregulated inflammation-resolution programs are associated with atherosclerosis progression. Resolvins, in part, mediate inflammation-resolution programs. Indeed, Resolvin D2 (RvD2) activates GPR18, a G-protein-coupled receptor, and limits plaque progression, though the cellular targets of RvD2 remain unknown. Here, we developed a humanized GPR18 floxed ("fl/fl") and a myeloid (Lysozyme M Cre) GPR18 knockout (mKO) mouse. We functionally validated this model by assessing efferocytosis in bone marrow-derived macrophages (BMDMs) and found that RvD2 enhanced efferocytosis in the fl/fl, but not in the mKO BMDMs. To understand the functions of RvD2-GPR18 in atherosclerosis, we performed a bone marrow transfer of fl/fl or mKO bone marrow into Ldlr
MeSH term(s)	Mice ; Animals ; Arginase ; Caspase 3 ; Macrophages ; Inflammation ; Atherosclerosis/genetics ; Necrosis ; Receptors, G-Protein-Coupled/genetics ; Docosahexaenoic Acids
Chemical Substances	resolvin D2 ; Arginase (EC 3.5.3.1) ; Caspase 3 (EC 3.4.22.-) ; GPR18 protein, mouse ; Receptors, G-Protein-Coupled ; Docosahexaenoic Acids (25167-62-8)
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202302336RR
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 296: Show issues

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Article: Resolvin D2-GPR18 Signaling on Myeloid Cells Limits Plaque Necrosis.

Lipscomb, Masharh / Walis, Sean / Marinello, Michael / Mena, Hebe Agustina / Spite, Matthew / Fredman, Gabrielle

bioRxiv : the preprint server for biology

2023

Abstract: Introduction/objective: Dysregulated inflammation-resolution programs are associated with atherosclerosis progression. Inflammation-resolution is in part mediated by Resolvins, including Resolvin D2 (RvD2). RvD2, which activates a G-protein coupled ... ...

Abstract	Introduction/objective: Dysregulated inflammation-resolution programs are associated with atherosclerosis progression. Inflammation-resolution is in part mediated by Resolvins, including Resolvin D2 (RvD2). RvD2, which activates a G-protein coupled receptor (GPCR) called GPR18, limits plaque progression. Cellular targets of RvD2 are not known. Approach and results: Here we developed humanized GPR18 floxed ("fl/fl") and a myeloid (Lysozyme M Cre) GPR18 knockout (mKO) mouse. We functionally validated this model by assessing efferocytosis in bone marrow derived macrophages (BMDMs) and found that RvD2 enhanced efferocytosis in the fl/fl, but not in the mKO BMDMs. We employed two different models to evaluate the role of GPR18 in atherosclerosis. We first used the PCSK9-gain of function approach and found increased necrosis in the plaques of the mKO mice compared with fl/fl mice. Next, we performed a bone marrow transfer of fl/fl or mKO bone marrow into Conclusions: These results are the first to suggest a causative role for endogenous RvD2 signaling on myeloid cells in limiting plaque necrosis. Moreover, these results provide a mechanistic basis for RvD2 as a therapy limiting plaque necrosis.
Language	English
Publishing date	2023-04-05
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.03.535493
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Article ; Online: Deciphering the role of n-3 polyunsaturated fatty acid-derived lipid mediators in health and disease.

Spite, Matthew

The Proceedings of the Nutrition Society

2013 Volume 72, Issue 4, Page(s) 441–450

Abstract: Accumulating evidence indicates that, analogous to n-6 PUFA, n-3 PUFA are enzymatically converted into diverse families of bioactive mediators that play numerous roles in physiology. These mediators, which include the resolvins, protectins and maresins, ... ...

Abstract	Accumulating evidence indicates that, analogous to n-6 PUFA, n-3 PUFA are enzymatically converted into diverse families of bioactive mediators that play numerous roles in physiology. These mediators, which include the resolvins, protectins and maresins, are particularly important in resolving acute inflammation and also appear to play a role in enhancing host defence. Given the protective actions of n-3 PUFA in human subjects and in animal models of disease, active generation of bioactive mediators may in part underlie these protective effects. Several studies have demonstrated that bioactive autacoids generated from n-3 PUFA have direct anti-inflammatory and pro-resolution actions, and the structures of many of these endogenous mediators have been elucidated. The diverse roles of these lipid mediators in health and disease, regulation of their biosynthesis, as well as identification of specific receptors and cellular targets, are emerging. This brief review will highlight the biosynthesis of resolvins, protectins and maresins, and discuss their receptor-mediated biological actions in promoting the resolution of inflammation. Their potential use as a new class of pro-resolution therapeutics, as well as gaps in knowledge and challenges for future research, will also be discussed. Overall, the identification of these novel families of lipid mediators has yielded insight into the protective actions of n-3 PUFA and may lead to the development of an entirely new class of therapeutics aimed at regulating inflammation and host defence.
MeSH term(s)	Docosahexaenoic Acids ; Fatty Acids, Omega-3/administration & dosage ; Fatty Acids, Omega-3/physiology ; Humans ; Immunomodulation ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation Mediators/physiology ; Lipid Metabolism/drug effects ; Randomized Controlled Trials as Topic
Chemical Substances	Fatty Acids, Omega-3 ; Inflammation Mediators ; Docosahexaenoic Acids (25167-62-8)
Language	English
Publishing date	2013-09-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	391142-1
ISSN	1475-2719 ; 0029-6651
ISSN (online)	1475-2719
ISSN	0029-6651
DOI	10.1017/S0029665113003030
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Article ; Online: Correction: Myeloid-Specific Deficiency of

Reeves, Andrew R / Sansbury, Brian E / Pan, Meixia / Han, Xianlin / Spite, Matthew / Greenberg, Andrew S

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 208, Issue 11, Page(s) 2593

Language	English
Publishing date	2022-05-16
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2200133
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Article ; Online: Effect of stretching on inflammation in a subcutaneous carrageenan mouse model analyzed at single-cell resolution.

Berrueta, Lisbeth / Muñoz-Vergara, Dennis / Martin, Daniel / Thompson, Rebecca / Sansbury, Brian E / Spite, Matthew / Badger, Gary J / Langevin, Helene M

Journal of cellular physiology

2023 Volume 238, Issue 12, Page(s) 2778–2793

Abstract: Understanding the factors that influence the biological response to inflammation is crucial, due to its involvement in physiological and pathological processes, including tissue repair/healing, cancer, infections, and autoimmune diseases. We have ... ...

Abstract	Understanding the factors that influence the biological response to inflammation is crucial, due to its involvement in physiological and pathological processes, including tissue repair/healing, cancer, infections, and autoimmune diseases. We have previously demonstrated that in vivo stretching can reduce inflammation and increase local pro-resolving lipid mediators in rats, suggesting a direct mechanical effect on inflammation resolution. Here we aimed to explore further the effects of stretching at the cellular/molecular level in a mouse subcutaneous carrageenan-inflammation model. Stretching for 10 min twice a day reduced inflammation, increased the production of pro-resolving mediator pathway intermediate 17-HDHA at 48 h postcarrageenan injection, and decreased both pro-resolving and pro-inflammatory mediators (e.g., PGE
MeSH term(s)	Animals ; Mice ; Carrageenan/metabolism ; Carrageenan/pharmacology ; Dinoprostone/metabolism ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Macrophages/metabolism ; Neutrophils/metabolism ; Single-Cell Analysis ; Mice, Inbred C57BL ; Transcriptome
Chemical Substances	Carrageenan (9000-07-1) ; Dinoprostone (K7Q1JQR04M) ; Inflammation Mediators
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.31133
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