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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Modulation of the anti-inflammatory effects of phosphatidylserine-containing liposomes by PEGylation.
TL;DR: Examining the effects of PEGylated phosphatidylserine-containing liposomes on the expression of two inflammation-associated cytokines indicates that PEG-PSLs can prevent TNF-α secretion without increasing TGF-β levels in macrophages, and they support the potential clinical use of PELs as anti-inflammatory agents with a relatively low potential to induce tissue fibrosis.
Journal ArticleDOI
Can phosphatidylserine enhance atheroprotective activities of high-density lipoprotein?
Maryam Darabi,Anatol Kontush +1 more
TL;DR: This review summarizes current knowledge about HDL-associated PS; possible mechanisms for its atheroprotective role are discussed and potential applications of PS to HDL-based therapies are highlighted.
Journal ArticleDOI
Soft apoptotic-cell-inspired nanoparticles persistently bind to macrophage membranes and promote anti-inflammatory and pro-healing effects.
TL;DR: In this article, a deformable deformable phosphatidylserine (PS)-containing nanoliposomes (D-PSLs) with a Young's modulus (E) of approximately 0.5 kPa were constructed via a facile and scalable method.
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Effects of RGD-grafted phosphatidylserine-containing liposomes on the polarization of macrophages and bone tissue regeneration.
Lele Wu,Yong-Joon Kim,Gyeung Mi Seon,Sang Hoon Choi,Heechul Park,Gitae Son,Soung Min Kim,Bum-Soon Lim,Hyeong-Cheol Yang +8 more
TL;DR: In this article, a 3% arginine-glycine-aspartic acid (RGD) peptide was used to enhance the phagocytosis of PSLs by macrophages.
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Effect of pegylated phosphatidylserine-containing liposomes in experimental chronic arthritis
Paulo C M Urbano,Vanete Thomaz Soccol,Vivian de Oliveira Nunes Teixeira,Patricia Gnieslaw de Oliveira,Lidiane Isabel Filippin,Wagner Hugo Bonat,Carolina de Oliveira,Gustavo Rodrigues Rossi,Ricardo Machado Xavier,Valderílio Feijó Azevedo +9 more
TL;DR: The experimental model showed an expression of severe arthritis after the booster of pegylated PSL, and PEG-PSL had no impact on the clinical score, the histopathology from tibial-tarsal joints or the production of cytokines in the knee joints.
References
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A protein kinase involved in the regulation of inflammatory cytokine biosynthesis.
Joseph C. Lee,Jeffrey T. Laydon,Peter C. McDonnell,Timothy Gallagher,Sanjay Kumar,David W. Green,Dean E. McNulty,M. J. Blumenthal,J. R. Heys,S. W. Landvatter,James E. Strickler,Megan M. McLaughlin,I. R. Siemens,Seth M. Fisher,George P. Livi,John R. White,Jerry L. Adams,Peter Young +17 more
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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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.