Phosphatidylserine-containing liposomes suppress inflammatory bone loss by ameliorating the cytokine imbalance provoked by infiltrated macrophages.
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TLDR
PSL-induced different influence on the activities of p38 MAPK and ERK is a likely underlying mechanism for phenotypic change of infiltrated macrophages after the phagocytosis of PSLs, resulting in the inhibition of inflammatory bone loss.About:
This article is published in Laboratory Investigation.The article was published on 2011-06-01 and is currently open access. It has received 52 citations till now. The article focuses on the topics: Interleukin 10 & Phagocytosis.read more
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Enhancing effect of sodium butyrate on phosphatidylserine–liposome-induced macrophage polarization
TL;DR: Sodium butyrate enhanced antiinflammatory properties and M2-polarization inducing effect of PSLs and may represent a novel approach to enhance PSL-induced macrophage polarization.
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Novel Mechanisms for Resolution of Liver Inflammation: Therapeutic Implications.
TL;DR: The discovery and understanding of the mechanisms by which inflammation is resolved are discussed and novel proresolving pathways that represent promising therapeutic strategies are highlighted.
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Phosphatidylserine enhances anti‐inflammatory effects of reconstituted HDL in macrophages via distinct intracellular pathways
TL;DR: In this article , the anti-inflammatory effects of PC/PS-rHDL were investigated in both tumor necrosis factor (TNF)-α- and lipopolysaccharide (LPS)-stimulated macrophages.
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DHA-enriched phosphatidylserine ameliorates high-fat diet-induced kidney injury in mice possibly by regulating TLR4/NF-κB and AMPK pathways.
Ya-fang Zhou,Shanshan Tian,Qiongfen Wang,Sijia Yao,Lingye Qian,Surong Jiang,Yuping Tang,T. Hand +7 more
TL;DR: Investigation of the amelioration effects of enzymatically synthesized docosahexaenoic acid-enriched phosphatidylserine on the high-fat diet (HFD)-induced kidney injury in mice suggested that improving serum or kidney parameters and regulating intestinal microbial could affect each other after DHA-PS treatment.
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Suppressive effects of an apoptotic mimicry prepared from jumbo-flying squid-skin phospholipids on the osteoclastogenesis in receptor activator of nuclear factor kappa B ligand/macrophage colony-stimulating factor-induced RAW 264.7 cells.
TL;DR: Current data support that a possible prevention of prepared SQ liposomes which are rich DHA and EPA on bone loss is through the suppression of osteoclastogenesis, and an in vivo study warrants a further investigation.
References
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TL;DR: Production of interleukin-1 and tumour necrosis factor from stimulated human monocytes is inhibited by a new series of pyridinyl-imidazole compounds, suggesting that the CSBPs are critical for cytokine production.
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Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.
TL;DR: The results suggest that binding and/or phagocytosis of apoptotic cells induces active antiinflammatory or suppressive properties in human macrophages, likely that resolution of inflammation depends not only on the removal of apoptosis but on active suppression of inflammatory mediator production.
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Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families.
TL;DR: Osteoblasts/stromal cells can now be replaced with RANKL and M-CSF in dealing with the whole life of osteoclasts, and new ways to treat several metabolic bone diseases caused by abnormal osteoclast recruitment and functions will be established.
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Resolution of inflammation: the beginning programs the end.
Charles N. Serhan,John Savill +1 more
TL;DR: Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins, and the mechanism required for inflammation resolution may underpin the development of drugs that can resolve inflammatory processes in directed and controlled ways.
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Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand
Young-Yun Kong,Ulrich Feige,Iidiko Sarosi,Brad Bolon,Anna Tafuri,Sean Morony,Casey Capparelli,Ji Li,Robin Elliott,Susan McCabe,Tom Wong,G Campagnuolo,Erika Moran,Earl R. Bogoch,Gwyneth Van,Linh T. Nguyen,Pamela S. Ohashi,David L. Lacey,Eleanor N. Fish,William J. Boyle,Josef M. Penninger,Josef M. Penninger +21 more
TL;DR: The results show that both systemic and local T-cell activation can lead to OPGL production and subsequent bone loss, and they provide a novel paradigm for T cells as regulators of bone physiology.