Milk Fat Globule‐Epidermal Growth Factor 8 (MFG‐E8) Is a Novel Anti‐inflammatory Factor in Rheumatoid Arthritis in Mice and Humans

ABSTRACT Milk fat globule‐epidermal growth factor 8 (MFG‐E8) is an anti‐inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in the pathogenesis of autoimmune and inflammatory diseases. Because MFG‐E8 also controls bone metabolism, we investigated its role in rh...

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Vydáno v:	Journal of bone and mineral research Ročník 31; číslo 3; s. 596 - 605
Hlavní autoři:	Albus, Elise, Sinningen, Kathrin, Winzer, Maria, Thiele, Sylvia, Baschant, Ulrike, Hannemann, Anke, Fantana, Julia, Tausche, Anne‐Kathrin, Wallaschofski, Henri, Nauck, Matthias, Völzke, Henry, Grossklaus, Sylvia, Chavakis, Triantafyllos, Udey, Mark C, Hofbauer, Lorenz C, Rauner, Martina
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England Oxford University Press 01.03.2016
Témata:	Aged Animals Anti-Inflammatory Agents - metabolism Antigens, Surface - blood Antigens, Surface - metabolism Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Bone Resorption - pathology Cytokines - metabolism Disease Progression Down-Regulation Female Humans INFLAMMATION Inflammation - pathology Inflammation Mediators - metabolism Joints - pathology Lipopolysaccharides Male MFG‐E8 Mice, Inbred C57BL Mice, Knockout Middle Aged Milk Proteins - blood Milk Proteins - metabolism Neutrophil Infiltration NEUTROPHILS; BONE LOSS RHEUMATOID ARTHRITIS Tumor Necrosis Factor-alpha RHEUMATOID ARTHRITIS MFG-E8 INFLAMMATION NEUTROPHILS; BONE LOSS
ISSN:	0884-0431, 1523-4681
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Abstract	ABSTRACT Milk fat globule‐epidermal growth factor 8 (MFG‐E8) is an anti‐inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in the pathogenesis of autoimmune and inflammatory diseases. Because MFG‐E8 also controls bone metabolism, we investigated its role in rheumatoid arthritis (RA), focusing on inflammation and joint destruction. The regulation of MFG‐E8 by inflammation was assessed in vitro using osteoblasts, in arthritic mice and in patients with RA. K/BxN serum transfer arthritis (STA) was applied to MFG‐E8 knock‐out mice to assess its role in the pathogenesis of arthritis. Stimulation of osteoblasts with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)‐α downregulated the expression of MFG‐E8 by 30% to 35%. MFG‐E8‐deficient osteoblasts responded to LPS with a stronger production of pro‐inflammatory cytokines. In vivo, MFG‐E8 mRNA levels were 52% lower in the paws of collagen‐induced arthritic (CIA) mice and 24% to 42% lower in the serum of arthritic mice using two different arthritis models (CIA and STA). Similarly, patients with RA (n = 93) had lower serum concentrations of MFG‐E8 (–17%) compared with healthy controls (n = 140). In a subgroup of patients who had a moderate to high disease activity (n = 21), serum concentrations of MFG‐E8 rose after complete or partial remission had been achieved (+67%). Finally, MFG‐E8‐deficient mice subjected to STA exhibited a stronger disease burden, an increased number of neutrophils in the joints, and a more extensive local and systemic bone loss. This was accompanied by an increased activation of osteoclasts and a suppression of osteoblast function in MFG‐E8‐deficient mice. Thus, MFG‐E8 is a protective factor in the pathogenesis of RA and subsequent bone loss. Whether MFG‐E8 qualifies as a novel biomarker or therapeutic target for the treatment of RA is worth addressing in further studies. © 2015 American Society for Bone and Mineral Research.
AbstractList	Milk fat globule-epidermal growth factor 8 (MFG-E8) is an anti-inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in the pathogenesis of autoimmune and inflammatory diseases. Because MFG-E8 also controls bone metabolism, we investigated its role in rheumatoid arthritis (RA), focusing on inflammation and joint destruction. The regulation of MFG-E8 by inflammation was assessed in vitro using osteoblasts, in arthritic mice and in patients with RA. K/BxN serum transfer arthritis (STA) was applied to MFG-E8 knock-out mice to assess its role in the pathogenesis of arthritis. Stimulation of osteoblasts with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α downregulated the expression of MFG-E8 by 30% to 35%. MFG-E8-deficient osteoblasts responded to LPS with a stronger production of pro-inflammatory cytokines. In vivo, MFG-E8 mRNA levels were 52% lower in the paws of collagen-induced arthritic (CIA) mice and 24% to 42% lower in the serum of arthritic mice using two different arthritis models (CIA and STA). Similarly, patients with RA (n = 93) had lower serum concentrations of MFG-E8 (-17%) compared with healthy controls (n = 140). In a subgroup of patients who had a moderate to high disease activity (n = 21), serum concentrations of MFG-E8 rose after complete or partial remission had been achieved (+67%). Finally, MFG-E8-deficient mice subjected to STA exhibited a stronger disease burden, an increased number of neutrophils in the joints, and a more extensive local and systemic bone loss. This was accompanied by an increased activation of osteoclasts and a suppression of osteoblast function in MFG-E8-deficient mice. Thus, MFG-E8 is a protective factor in the pathogenesis of RA and subsequent bone loss. Whether MFG-E8 qualifies as a novel biomarker or therapeutic target for the treatment of RA is worth addressing in further studies. Milk fat globule-epidermal growth factor 8 (MFG-E8) is an anti-inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in the pathogenesis of autoimmune and inflammatory diseases. Because MFG-E8 also controls bone metabolism, we investigated its role in rheumatoid arthritis (RA), focusing on inflammation and joint destruction. The regulation of MFG-E8 by inflammation was assessed in vitro using osteoblasts, in arthritic mice and in patients with RA. K/BxN serum transfer arthritis (STA) was applied to MFG-E8 knock-out mice to assess its role in the pathogenesis of arthritis. Stimulation of osteoblasts with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)- alpha downregulated the expression of MFG-E8 by 30% to 35%. MFG-E8-deficient osteoblasts responded to LPS with a stronger production of pro-inflammatory cytokines. In vivo, MFG-E8 mRNA levels were 52% lower in the paws of collagen-induced arthritic (CIA) mice and 24% to 42% lower in the serum of arthritic mice using two different arthritis models (CIA and STA). Similarly, patients with RA (n=93) had lower serum concentrations of MFG-E8 (-17%) compared with healthy controls (n=140). In a subgroup of patients who had a moderate to high disease activity (n=21), serum concentrations of MFG-E8 rose after complete or partial remission had been achieved (+67%). Finally, MFG-E8-deficient mice subjected to STA exhibited a stronger disease burden, an increased number of neutrophils in the joints, and a more extensive local and systemic bone loss. This was accompanied by an increased activation of osteoclasts and a suppression of osteoblast function in MFG-E8-deficient mice. Thus, MFG-E8 is a protective factor in the pathogenesis of RA and subsequent bone loss. Whether MFG-E8 qualifies as a novel biomarker or therapeutic target for the treatment of RA is worth addressing in further studies. . Milk fat globule-epidermal growth factor 8 (MFG-E8) is an anti-inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in the pathogenesis of autoimmune and inflammatory diseases. Because MFG-E8 also controls bone metabolism, we investigated its role in rheumatoid arthritis (RA), focusing on inflammation and joint destruction. The regulation of MFG-E8 by inflammation was assessed in vitro using osteoblasts, in arthritic mice and in patients with RA. K/BxN serum transfer arthritis (STA) was applied to MFG-E8 knock-out mice to assess its role in the pathogenesis of arthritis. Stimulation of osteoblasts with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-[alpha] downregulated the expression of MFG-E8 by 30% to 35%. MFG-E8-deficient osteoblasts responded to LPS with a stronger production of pro-inflammatory cytokines. In vivo, MFG-E8 mRNA levels were 52% lower in the paws of collagen-induced arthritic (CIA) mice and 24% to 42% lower in the serum of arthritic mice using two different arthritis models (CIA and STA). Similarly, patients with RA (n=93) had lower serum concentrations of MFG-E8 (-17%) compared with healthy controls (n=140). In a subgroup of patients who had a moderate to high disease activity (n=21), serum concentrations of MFG-E8 rose after complete or partial remission had been achieved (+67%). Finally, MFG-E8-deficient mice subjected to STA exhibited a stronger disease burden, an increased number of neutrophils in the joints, and a more extensive local and systemic bone loss. This was accompanied by an increased activation of osteoclasts and a suppression of osteoblast function in MFG-E8-deficient mice. Thus, MFG-E8 is a protective factor in the pathogenesis of RA and subsequent bone loss. Whether MFG-E8 qualifies as a novel biomarker or therapeutic target for the treatment of RA is worth addressing in further studies. © 2015 American Society for Bone and Mineral Research. ABSTRACT Milk fat globule‐epidermal growth factor 8 (MFG‐E8) is an anti‐inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in the pathogenesis of autoimmune and inflammatory diseases. Because MFG‐E8 also controls bone metabolism, we investigated its role in rheumatoid arthritis (RA), focusing on inflammation and joint destruction. The regulation of MFG‐E8 by inflammation was assessed in vitro using osteoblasts, in arthritic mice and in patients with RA. K/BxN serum transfer arthritis (STA) was applied to MFG‐E8 knock‐out mice to assess its role in the pathogenesis of arthritis. Stimulation of osteoblasts with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)‐α downregulated the expression of MFG‐E8 by 30% to 35%. MFG‐E8‐deficient osteoblasts responded to LPS with a stronger production of pro‐inflammatory cytokines. In vivo, MFG‐E8 mRNA levels were 52% lower in the paws of collagen‐induced arthritic (CIA) mice and 24% to 42% lower in the serum of arthritic mice using two different arthritis models (CIA and STA). Similarly, patients with RA (n = 93) had lower serum concentrations of MFG‐E8 (–17%) compared with healthy controls (n = 140). In a subgroup of patients who had a moderate to high disease activity (n = 21), serum concentrations of MFG‐E8 rose after complete or partial remission had been achieved (+67%). Finally, MFG‐E8‐deficient mice subjected to STA exhibited a stronger disease burden, an increased number of neutrophils in the joints, and a more extensive local and systemic bone loss. This was accompanied by an increased activation of osteoclasts and a suppression of osteoblast function in MFG‐E8‐deficient mice. Thus, MFG‐E8 is a protective factor in the pathogenesis of RA and subsequent bone loss. Whether MFG‐E8 qualifies as a novel biomarker or therapeutic target for the treatment of RA is worth addressing in further studies. © 2015 American Society for Bone and Mineral Research.
Author	Chavakis, Triantafyllos Völzke, Henry Albus, Elise Grossklaus, Sylvia Thiele, Sylvia Sinningen, Kathrin Hannemann, Anke Winzer, Maria Hofbauer, Lorenz C Baschant, Ulrike Fantana, Julia Udey, Mark C Nauck, Matthias Tausche, Anne‐Kathrin Wallaschofski, Henri Rauner, Martina
AuthorAffiliation	4 Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany 3 Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany 2 Department of Obstetrics and Gynecology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany 5 Department of Clinical Pathobiochemistry and Institute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany 6 DFG Research Center for Regenerative Therapies Dresden, Dresden, Germany 1 Department of Medicine III, Technische Universität Dresden, Dresden, Germany 7 Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
AuthorAffiliation_xml	– name: 5 Department of Clinical Pathobiochemistry and Institute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany – name: 1 Department of Medicine III, Technische Universität Dresden, Dresden, Germany – name: 6 DFG Research Center for Regenerative Therapies Dresden, Dresden, Germany – name: 3 Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany – name: 7 Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA – name: 2 Department of Obstetrics and Gynecology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany – name: 4 Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany
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Keywords	RHEUMATOID ARTHRITIS MFG-E8 INFLAMMATION NEUTROPHILS; BONE LOSS
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Authors’ roles: Study design: EA, KS, MW, LCH, and MR. Study conduct: EA, KS, MW, and ST. Data collection, analysis, and interpretation: all authors. Drafting manuscript: EA, KS, MW, LCH, and MR. Revising manuscript content and approving final version of manuscript: all authors. MR takes responsibility for the integrity of the data analysis. EA, KS, and MW contributed equally to this work.
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Snippet	ABSTRACT Milk fat globule‐epidermal growth factor 8 (MFG‐E8) is an anti‐inflammatory glycoprotein that mediates the clearance of apoptotic cells and is... Milk fat globule-epidermal growth factor 8 (MFG-E8) is an anti-inflammatory glycoprotein that mediates the clearance of apoptotic cells and is implicated in...
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SubjectTerms	Aged Animals Anti-Inflammatory Agents - metabolism Antigens, Surface - blood Antigens, Surface - metabolism Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Bone Resorption - pathology Cytokines - metabolism Disease Progression Down-Regulation Female Humans INFLAMMATION Inflammation - pathology Inflammation Mediators - metabolism Joints - pathology Lipopolysaccharides Male MFG‐E8 Mice, Inbred C57BL Mice, Knockout Middle Aged Milk Proteins - blood Milk Proteins - metabolism Neutrophil Infiltration NEUTROPHILS; BONE LOSS RHEUMATOID ARTHRITIS Tumor Necrosis Factor-alpha
Title	Milk Fat Globule‐Epidermal Growth Factor 8 (MFG‐E8) Is a Novel Anti‐inflammatory Factor in Rheumatoid Arthritis in Mice and Humans
URI	https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjbmr.2721 https://www.ncbi.nlm.nih.gov/pubmed/26391522 https://www.proquest.com/docview/1776618187 https://www.proquest.com/docview/1777488543 https://www.proquest.com/docview/1780521582 https://pubmed.ncbi.nlm.nih.gov/PMC6999704
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