Resolvins E1 and D1 in Choroid-Retinal Endothelial Cells and Leukocytes: Biosynthesis and Mechanisms of Anti-inflammatory Actions

Tian, Haibin; Lü, Yan; Sherwood, Alexander M.; Hongqian, Dawuti; Hong, Song

doi:10.1167/iovs.08-3146

Cited by 70 publications

(62 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, VCAM-1 immunoneutralization has shown higher therapeutic effects than that of ICAM-1 in experimental colitis (49). Furthermore, our findings are in line with previous studies that have shown that RvE1 and RvD1 reduce PMN transmigration across choroid retinal endothelial cells stimulated with IL-1b and that this effect is dependent on VCAM-1 expression (50). In addition, in vitro incubation with EPA or DHA has been shown to decrease VCAM-1, ICAM-1, and LFA-1 expression in human epithelial cells stimulated with LPS (51).…”

Section: Discussionsupporting

confidence: 92%

Omega-3 Fatty Acid-Derived Mediators 17(R)-Hydroxy Docosahexaenoic Acid, Aspirin-Triggered Resolvin D1 and Resolvin D2 Prevent Experimental Colitis in Mice

Bento

Claudino

Dutra

et al. 2011

The Journal of Immunology

226

193

View full text Add to dashboard Cite

Resolvins of the D series are generated from docosahexaenoic acid, which are enriched in fish oils and are believed to exert beneficial roles on diverse inflammatory disorders, including inflammatory bowel disease (IBD). In this study, we investigated the anti-inflammatory effects of the aspirin-triggered resolvin D1 (AT-RvD1), its precursor (17(R)-hydroxy docosahexaenoic acid [17R-HDHA]) and resolvin D2 (RvD2) in dextran sulfate sodium (DSS)- or 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Our results showed that the systemic treatment with AT-RvD1, RvD2, or 17R-HDHA in a nanogram range greatly improved disease activity index, body weight loss, colonic damage, and polymorphonuclear infiltration in both colitis experimental models. Moreover, these treatments reduced colonic cytokine levels for TNF-α, IL-1β, MIP-2, and CXCL1/KC, as well as mRNA expression of NF-κB and the adhesion molecules VCAM-1, ICAM-1, and LFA-1. Furthermore, AT-RvD1, but not RvD2 or 17R-HDHA, depended on lipoxin A4 receptor (ALX) activation to inhibit IL-6, MCP-1, IFN-γ, and TNF-α levels in bone marrow-derived macrophages stimulated with LPS. Similarly, ALX blockade reversed the beneficial effects of AT-RvD1 in DSS-induced colitis. To our knowledge, our findings showed for the first time the anti-inflammatory effects of resolvins of the D series and precursor 17R-HDHA in preventing experimental colitis. We also demonstrated the relevant role exerted by ALX activation on proresolving action of AT-RvD1. Moreover, AT-RvD1 showed a higher potency than 17R-HDHA and RvD2 in preventing DSS-induced colitis. The results suggest that these lipid mediators possess a greater efficacy when compared with other currently used IBD therapies, such as monoclonal anti-TNF, and have the potential to be used for treating IBD.

show abstract

Section: Discussionsupporting

confidence: 92%

Omega-3 Fatty Acid-Derived Mediators 17(R)-Hydroxy Docosahexaenoic Acid, Aspirin-Triggered Resolvin D1 and Resolvin D2 Prevent Experimental Colitis in Mice

Bento

Claudino

Dutra

et al. 2011

The Journal of Immunology

226

193

View full text Add to dashboard Cite

show abstract

“…macrophages in vitro. Decrease in IL-8, a potent PMN chemoattractant, has also been shown for other SPMs, including RvD1, 25 and is consistent with the decrease in PMN levels during bacterial infection (Figures 2 and 6). The reduction in tumor necrosis factor-a and IL-6 (pyrogenic cytokines) is an action also shared with RvD1, RvD2, and RvD3.…”

Section: Discussionsupporting

confidence: 84%

The Protectin PCTR1 Is Produced by Human M2 Macrophages and Enhances Resolution of Infectious Inflammation

Ramon

Dalli

Sanger

et al. 2016

The American Journal of Pathology

115

View full text Add to dashboard Cite

Inflammation and its natural resolution are host-protective responses triggered by infection or injury. The resolution phase of inflammation is regulated by enzymatically produced specialized pro-resolving mediators. We recently identified a new class of peptide-conjugated specialized pro-resolving mediators that carry potent tissue regenerative actions that belong to the protectin family and are coined protectin conjugates in tissue regeneration (PCTR). Herein, with the use of microbial-induced peritonitis in mice and liquid chromatography-tandem mass spectrometryebased lipid mediator metabololipidomics, we found that PCTR1 is temporally regulated during self-resolving infection. When administered at peak of inflammation, PCTR1 enhanced macrophage recruitment and phagocytosis of Escherichia coli, decreased polymorphonuclear leukocyte infiltration, and counter-regulated inflammation-initiating lipid mediators, including prostaglandins. In addition, biologically produced PCTR1 promoted human monocyte and macrophage migration in a dose-dependent manner (0.001 to 10.0 nmol/L). We prepared PCTR1 via organic synthesis and confirmed that synthetic PCTR1 increased macrophage and monocyte migration, enhanced macrophage efferocytosis, and accelerated tissue regeneration in planaria. With human macrophage subsets, PCTR1 levels were significantly higher in M2 macrophages than in M1 phenotype, along with members of the resolvin conjugates in tissue regeneration and maresin conjugate families. In contrast, M1 macrophages gave higher levels of cysteinyl leukotrienes. Together, these results demonstrate that PCTR1 is a potent monocyte/macrophage agonist, regulating key anti-inflammatory and pro-resolving processes during bacterial infection. (Am J Pathol 2016, 186: 962e973; http://dx

show abstract

“…20,21 Briefly, peripheral blood samples were mixed with the same volume of PBS containing 4% dextran and were centrifuged at 150 ϫ g for 15 minutes. Platelet-rich supernatant was further centrifuged at 1600 ϫ g for 15 minutes to collect platelets.…”

Section: Cell Culturesmentioning

confidence: 99%

“…They also likely enhance 12/15-lipoxygenase-like activity, 26 which results in 14-hydroxylation of DHA and some DHA derivatives. 20 Each incubation was extracted for analysis and preparative separation of 14S,21R-diHDHA or its biosynthetic intermediates. The pH of each incubation was adjusted to pH 4.5 with HCl (1 mol/L, on ice) and then the incubation was mixed with three volumes of ice-cold methanol (sample:methanol ϭ 1:3 v/v).…”

Section: Cell Culturesmentioning

confidence: 99%

Autacoid 14S,21R-Dihydroxy-Docosahexaenoic Acid Counteracts Diabetic Impairment of Macrophage Prohealing Functions

Tian

Lü

Shah

et al. 2011

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

Impaired macrophage functions imposed by diabetic complications and the suppressed formation of 14S, 2 1 R -d i h y d r o x y d o c o s a -4 Z , 7Z , 1 0 Z , 1 2 E , 1 6 Z , 19Z-hexaenoic acid (14S,21R-diHDHA) in wounds contribute significantly to deficient wound healing in diabetics, but how are macrophage functions and 14S,21R-diHDHA formation associated? We studied 14S,21R-diHDHA generation from macrophages using liquid chromatography/mass spectrometry. The role in macrophage-mediated wound healing functions was determined using a murine splinted excisional wound healing model and in vitro assays. 14S,21R-diHDHA acts as a macrophage-generated autacoid, and its attenuated formation in macrophages of diabetic db/db mice was accompanied by impairment of macrophage prohealing functions. 14S,21R-diHDHA restored db/db macrophage-impaired prohealing functions by promoting wound re-epithelialization, formulation of granulation tissue, and vascularization. Additionally, 12/15-lipoxygenase-deficient macrophages, which are unable to produce 14S,21R-diHDHA, exhibited impaired prohealing functions, which also were restored by 14S,21R-diHDHA treatment. The molecular mechanism for 14S,21R-diHDHA-induced recovery of impaired prohealing functions of db/db macrophages involves enhancing their secretion of vascular endothelial growth factor and platelet-derived growth factor BB, decreasing hyperglycemia-induced generation of reactive oxygen species, and increasing IL-10 expression under inflammatory stimulation. Taken together, these results indicate that deficiency of 14S,21R-diHDHA formation by diabetic macrophages contributes to their impaired prohealing functions. Our findings provide mechanistic insights into wound healing in diabetics and suggest the possibility of using autologous macrophages/monocytes, treated with 14S,21R-diHDHA, or related compounds, to promote diabetes-impaired wound healing. (Am J Pathol

show abstract

Resolvins E1 and D1 in Choroid-Retinal Endothelial Cells and Leukocytes: Biosynthesis and Mechanisms of Anti-inflammatory Actions

Cited by 70 publications

References 45 publications

Omega-3 Fatty Acid-Derived Mediators 17(R)-Hydroxy Docosahexaenoic Acid, Aspirin-Triggered Resolvin D1 and Resolvin D2 Prevent Experimental Colitis in Mice

Omega-3 Fatty Acid-Derived Mediators 17(R)-Hydroxy Docosahexaenoic Acid, Aspirin-Triggered Resolvin D1 and Resolvin D2 Prevent Experimental Colitis in Mice

The Protectin PCTR1 Is Produced by Human M2 Macrophages and Enhances Resolution of Infectious Inflammation

Autacoid 14S,21R-Dihydroxy-Docosahexaenoic Acid Counteracts Diabetic Impairment of Macrophage Prohealing Functions

Contact Info

Product

Resources

About