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Open AccessJournal ArticleDOI

Phosphatidylserine-containing liposomes suppress inflammatory bone loss by ameliorating the cytokine imbalance provoked by infiltrated macrophages.

Hong Mei Ma, +2 more
- 01 Jun 2011 - 
- Vol. 91, Iss: 6, pp 921-931
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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.

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Citations
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Journal ArticleDOI

Pathways for Bone Loss in Inflammatory Disease

TL;DR: This review summarizes new data on inflammatory bone loss obtained in 2011 and describes the molecular pathways by which receptor activator of nuclear factor-κB ligand and RANKL induce osteoclast differentiation.
Journal ArticleDOI

HCMV reprogramming of infected monocyte survival and differentiation: a Goldilocks phenomenon.

TL;DR: The induction of a uniquely polarized macrophage subset from infected monocytes is described, which is argued to be the ideal cellular environment for the initiation of viral gene expression and replication and, ultimately, viral spread and persistence within the infected host.
Journal ArticleDOI

Myelin alters the inflammatory phenotype of macrophages by activating PPARs

TL;DR: The data show that myelin modulates the phenotype of macrophages by PPAR activation, which may subsequently dampen MS lesion progression and the immunoregulatory impact of naturally-occurring myelin lipids may hold promise for future MS therapeutics.
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Anti-obesity and anti-inflammatory effects of macrophage-targeted interleukin-10-conjugated liposomes in obese mice.

TL;DR: The findings suggest that the PSL-IL10 has macrophage targeting ability and enhanced anti- inflammatory effect due to the synergistic anti-inflammatory effects of IL-10 and PSL, and can be used as amacrophage-targeted therapeutic material for inflammation-related diseases, including obesity.
References
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Journal ArticleDOI

Phosphatidylserine-dependent ingestion of apoptotic cells promotes TGF-β1 secretion and the resolution of inflammation

TL;DR: In vivo that direct instillation of apoptotic cells enhanced the resolution of acute inflammation, and apoptotic cell recognition and clearance, via exposure of PS and ligation of its receptor, induce TGF-beta1 secretion, resulting in accelerated resolution of inflammation.
Journal ArticleDOI

Modulation of Osteoclast Differentiation

TL;DR: Osteotropic hormones such as 1α, 25-dihydroxyvitamin D3 [1α,25(OH)2D3], PTH, and calcitonin preferentially modulate the process of bone resorption to maintain bone remodeling.
Journal ArticleDOI

Resolution of inflammation: state of the art, definitions and terms.

TL;DR: A consensus report was needed that addresses the rapid progress in this emerging field and details how the specific study of resolution of acute inflammation provides leads for novel anti‐inflammatory therapeutics, as well as defines the terms and key components of interest in the resolution process within tissues as appreciated today.
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Endotoxin signal transduction in macrophages

TL;DR: The effects of LPS on macrophages are examined by following events from the cell surface to the nucleus and the involvement of protein tyrosine kinase, mitogen‐activated protein kinases, protein kinase C, G proteins, Protein kinase A, ceramide‐activatedprotein kinase and microtubules in this process are reviewed.
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