Haemopoietic biglycan produced by brain cells stimulates growth of microglial cells

Kikuchi, Azusa; Tomoyasu, Hiroshi; Kido, Isao; Takahashi, Kazuhiro; Tanaka, Akio; Nonaka, Ikuya; Iwakami, Noboru; Kamo, Isao

doi:10.1016/s0165-5728(99)00258-1

Cited by 27 publications

(29 citation statements)

References 34 publications

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“…Second, biglycan is reported to stimulate growth and differentiation of monocytic cells, suggesting a hemopoietic role for this proteoglycan. 39 PG-MCSF is a proteoglycan form of a known factor that promotes growth and differentiation of mononuclear phagocytic cells. 40 It will be of interest to compare the lipoprotein-binding and hemopoietic properties of these 2 proteoglycans whose synthesis is responsive to lysoPC.…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidylcholine Regulates Synthesis of Biglycan and the Proteoglycan Form of Macrophage Colony Stimulating Factor

Chang

Tsoi

Wight

et al. 2003

ATVB

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Objective-We have shown that copper-oxidized LDL (Ox-LDL) regulates proteoglycan synthesis by arterial smooth muscle cells. Ox-LDL specifically upregulates biglycan expression while causing elongation of glycosaminoglycan chains on all of the major secreted proteoglycans (biglycan, decorin, and versican), resulting in enhanced lipoproteinbinding interactions. It is not known which component of Ox-LDL is responsible for these effects. This study investigated the ability of several bioactive components of Ox-LDL to regulate proteoglycan synthesis. Methods and Results-Those tested included 2 oxysterols (7-ketocholesterol and 7␤-hydroxycholesterol) and 2 lysolipids (lysophosphatidylcholine and lysophosphatidic acid) formed during LDL oxidation. 7-ketocholesterol, lysophosphatidylcholine, and lysophosphatidic acid all increased proteoglycan MW app , which is correlated with chain elongation and enhanced lipoprotein-binding properties in vitro. Lysophosphatidylcholine mimics the ability of Ox-LDL to stimulate biglycan expression and also causes a marked induction of the core protein for the proteoglycan form of macrophage colony stimulating factor. Key Words: lysophosphatidylcholine Ⅲ oxidized LDL Ⅲ proteoglycan Ⅲ biglycan Ⅲ proteoglycan form of macrophage colony stimulating factor T he interactions of proteoglycans with LDL are hypothesized to be the major cause of extracellular lipid accumulation within atherosclerotic lesions. 1-3 Such proteoglycan-mediated lipid accumulation can be attributable to either direct interaction between these molecules or indirect interaction via bridging molecules. 4,5 Several consequences result that potentially contribute to atherogenesis, including increased susceptibility of lipoproteins to oxidation 6 or aggregation 7 and rapid internalization of lipoproteinproteoglycan complexes by both macrophages and smooth muscle cells. 6 Conclusions-Multiple

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Section: Discussionmentioning

confidence: 99%

Lysophosphatidylcholine Regulates Synthesis of Biglycan and the Proteoglycan Form of Macrophage Colony Stimulating Factor

Chang

Tsoi

Wight

et al. 2003

ATVB

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“…Biglycan stimulates the development, growth and differentiation in cells of the monocytic lineage. 64 Furthermore, biglycan strongly binds to the complement factor C1q 65 with yet-unknown biological consequences. It acts as a ligand of CD44 and thereby appears to be involved in the recruitment of CD16-negative natural killer cells.…”

Section: Interaction Of Biglycan With Tlr2/4 In Pathogen-mediated Andmentioning

confidence: 99%

Small leucine-rich proteoglycans orchestrate receptor crosstalk during inflammation

2012

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“…Smooth muscle cells exposed to lysoPC also secreted the proteoglycan form of monocyte-macrophage colony-stimulating factor (M-CSF), the predominant proteoglycan produced by macrophages (121). M-CSF may play a role in lipoprotein retention and macrophage maturation and differentiation (122).…”

Section: Saamentioning

confidence: 99%

Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?

Chait

Oram

Heinecke

2005

Journal of Lipid Research

209

159

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In humans, a chronically increased circulating level of C-reactive protein (CRP), a positive acute-phase reactant, is an independent risk factor for cardiovascular disease. This observation has led to considerable interest in the role of inflammatory proteins in atherosclerosis. In this review, after discussing CRP, we focus on the potential role in the pathogenesis of human vascular disease of inflammation-induced proteins that are carried by lipoproteins. Serum amyloid A (SAA) is transported predominantly on HDL, and levels of this protein increase markedly during acute and chronic inflammation in both animals and humans. Increased SAA levels predict the risk of cardiovascular disease in humans. Recent animal studies support the proposal that SAA plays a role in atherogenesis. Evidence is accruing that secretory phospholipase A 2 , an HDL-associated protein, and platelet-activating factor acetylhydrolase, a protein associated predominantly with LDL in humans and HDL in mice, might also play roles both as markers and mediators of human atherosclerosis. In contrast to positive acute-phase proteins, which increase in abundance during inflammation, negative acutephase proteins have received less attention. Apolipoprotein A-I (apoA-I), the major apolipoprotein of HDL, decreases during inflammation. Recent studies also indicate that HDL is oxidized by myeloperoxidase in patients with established atherosclerosis. These alterations may limit the ability of apoA-I to participate in reverse cholesterol transport. Paraoxonase-1 (PON1), another HDL-associated protein, also decreases during inflammation. PON1 is atheroprotective in animal models of hypercholesterolemia. Controversy over its utility as a marker of human atherosclerosis may reflect the fact that enzyme activity rather than blood level (or genotype) is the major determinant of cardiovascular risk. Thus, multiple lipoprotein-associated proteins that change in concentration during acute and chronic inflammation may serve as markers of cardiovascular disease. In future studies, it will be important to determine whether these proteins play a causal role in atherogenesis.

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Haemopoietic biglycan produced by brain cells stimulates growth of microglial cells

Cited by 27 publications

References 34 publications

Lysophosphatidylcholine Regulates Synthesis of Biglycan and the Proteoglycan Form of Macrophage Colony Stimulating Factor

Lysophosphatidylcholine Regulates Synthesis of Biglycan and the Proteoglycan Form of Macrophage Colony Stimulating Factor

Small leucine-rich proteoglycans orchestrate receptor crosstalk during inflammation

Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?

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