C-reactive protein-induced upregulation of extracellular matrix metalloproteinase inducer in macrophages: Inhibitory effect of fluvastatin

Abe, Naoki; Osanai, Tomohiro; Fujiwara, Takayuki; Kameda, Kunihiko; Matsunaga, Toshiro; Okumura, Ken

doi:10.1016/j.lfs.2005.06.015

Cited by 49 publications

(36 citation statements)

References 28 publications

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“…Because endotoxin is a well-known macrophage LPL inhibitory factor (28), endotoxin contamination of the CRP preparation may not account for this effect. Our findings that low CRP concentrations induce optimal macrophage LPL expression compare well with the results of previous studies showing that a triggering signal provided by 1 to 10 mg/ml CRP induces maximal macrophage tumoricidal activity, MMP-9 expression, and CSF and interleukin-1a production (5,7,8,10).…”

Section: Discussionsupporting

confidence: 91%

“…Interaction of CRP with these cells induces an increase in the secretion of inflammatory mediators such as cytokines and chemokines (5,6). Additional effects of CRP on monocytes/macrophages include induction of colony stimulating factor (CSF), matrix metalloproteinase (MMP), nitric oxide, and tumoricidal activity (7)(8)(9)(10). Most importantly, CRP also appears to promote infiltration of monocytes into the vessel wall (11) and their subsequent development into foam cells (12).…”

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confidence: 99%

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C-reactive protein enhances macrophage lipoprotein lipase expression

Maingrette

Renier

2008

Journal of Lipid Research

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High serum levels of C-reactive protein (CRP), a strong predictor of cardiovascular events, are documented in patients with type 2 diabetes. Accumulating evidence suggests that CRP could directly promote arterial damage. To determine the role of CRP in diabetic atherosclerosis, we examined the effect of CRP on the expression of macrophage lipoprotein lipase (LPL), a proatherogenic molecule upregulated in type 2 diabetes. Treatment of human macrophages with native CRP increased, in a dose-and timedependent manner, LPL protein expression and secretion. Modified CRP reproduced these effects. Preincubation of human macrophages with antioxidants, protein kinase C (PKC), and mitogen-activated protein kinase (MAPK) inhibitors prevented CRP-induced LPL expression. Exposure of human macrophages to CRP further increased intracellular reactive oxygen species generation, classic PKC isozymes expression, and extracellular signal-regulated protein kinase 1/2 phosphorylation. In CRP-treated J774 macrophages, increased macrophage LPL mRNA levels and enhanced binding of nuclear proteins to the activated protein-1 (AP-1)-enhancing element were observed. These effects were prevented by antioxidants, as well as by PKC, MAPK, and AP-1 inhibitors. These data show for the first time that CRP directly increases macrophage LPL expression and secretion. Given the predominant role of macrophage LPL in atherogenesis, LPL might represent a novel factor underlying the adverse effect of CRP on the diabetic vasculature.-Maingrette, F., L. Li, and G. Renier. C-reactive protein enhances macrophage lipoprotein lipase expression. J. Lipid Res. 2008Res. . 49: 1926Res. -1935 Since the hypothesis that inflammation might be an accomplice in the pathogenesis of atherosclerosis and type 2 diabetes was first proposed, many epidemiological and clinical studies have shown that circulating markers of inflammation predict the risk of future cardiovascular (CV) events and type 2 diabetes and that an ongoing acute phase response is present in patients with type 2 diabetes (1). In addition to being a CV risk marker (2, 3), C-reactive protein (CRP) could also make a direct contribution to the atherosclerotic process. Supporting this possibility, it has been shown that CRP is present in the plaque (4) and that exposure of cultured vascular cells to CRP leads to various proinflammatory and proatherogenic effects. Among the cell types found in the lesion, monocytes/macrophages have essential functions in all phases of atherosclerosis. Interaction of CRP with these cells induces an increase in the secretion of inflammatory mediators such as cytokines and chemokines (5, 6). Additional effects of CRP on monocytes/macrophages include induction of colony stimulating factor (CSF), matrix metalloproteinase (MMP), nitric oxide, and tumoricidal activity (7-10). Most importantly, CRP also appears to promote infiltration of monocytes into the vessel wall (11) and their subsequent development into foam cells (12).Lipoprotein lipase (LPL) is a key enzyme in the hydro...

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Section: Discussionsupporting

confidence: 91%

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confidence: 99%

C-reactive protein enhances macrophage lipoprotein lipase expression

Maingrette

Renier

2008

Journal of Lipid Research

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“…Also, CRP in vitro is reported to promote the production of several MMPs, such as MMP-9 in mononuclear cells (16) and rat peritoneal macrophages (17) as well as MMP-1 in U937 histiocytes and human monocyte-derived macrophages (18). CRP-mediated MMP induction has been reported at multiple levels, such as p38 MAPK and the synergistic action of p38 and JNK for MMP-1 and MMP-10, respectively, in HAECs and human cornorary artery endothelial cells (19), the MAPK pathway for MMP-2 in human vascular smooth muscle cells (20), ERK for MMP-1 in U937 histiocytes (18), NADPH oxidase for MMP-9 release in rat macrophages (17), and the CD40-CD40L signaling pathway for the induction of MMP-2 and MMP-9 (21). Additionally, the use of function-blocking antibodies to TNF-a and IL-1b has been reported to significantly inhibit the induction of MMP-9 in human mononuclear cells (16).…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, MMP-1 (a collagenase), MMP-2 (a gelatinase), and MMP-3 (a stromelysin) are predominantly secreted by endothelial cells (14), whereas the major MMP secreted from macrophages is MMP-9 (a gelatinase) (15). Also, CRP has been reported to induce the release of various different forms of MMP from the cells involved in the process of atherogenesis (16)(17)(18)(19)(20)(21).…”

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confidence: 99%

Human C-reactive protein promotes oxidized low density lipoprotein uptake and matrix metalloproteinase-9 release in Wistar rats

Singh

Dasu

Yancey

et al. 2008

Journal of Lipid Research

104

117

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C-reactive protein (CRP) is present in the atherosclerotic plaques and appears to promote atherogenesis. Intraplaque CRP colocalizes with oxidized low density lipoprotein (OxLDL) and macrophages in human atherosclerotic lesions. Matrix metalloproteinase-9 (MMP-9) has been implicated in plaque rupture. CRP promotes OxLDL uptake and MMP induction in vitro; however, these have not been investigated in vivo. We examined the effect of CRP on OxLDL uptake and MMP-9 production in vivo in Wistar rats. CRP significantly increased OxLDL uptake in the peritoneal and sterile pouch macrophages compared with human serum albumin (huSA). CRP also significantly increased intracellular cholesteryl ester accumulation compared with huSA. The increased uptake of OxLDL by CRP was inhibited by pretreatment with antibodies to CD32, CD64, CD36, and fucoidin, suggesting uptake by both scavenger receptors and Fc-g receptors. Furthermore, CRP treatment increased MMP-9 activity in macrophages compared with huSA, which was abrogated by inhibitors to p38 mitogen-activated protein kinase, extracellular signalregulated kinase (ERK), and nuclear factor (NF)-kB but not Jun N-terminal kinase ( JNK ) before human CRP treatment. Because OxLDL uptake by macrophages contributes to foam cell formation and MMP release contributes to plaque instability, this study provides novel in vivo evidence for the role of CRP in atherosclerosis.-Singh, U., M. R. Dasu, P. G. Yancey, A. Afify, S. Devaraj, and I. Jialal. Human C-reactive protein promotes oxidized low density lipoprotein uptake and matrix metalloproteinase-9 release in Wistar rats.

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“…The transcribed cDNA was amplified by PCR with specific primers for procollagen α 1(I), procollagen α 1(III), tropoelastin, p22phox, SAP, MMP-2, MMP-9, and glyceraldehydes-3-phosphate dehydrogenase (GAPDH). Two specific primer pairs corresponding to published sequences were used to amplify procollagen α 1(I) (5 ′ -CAGCCGCTTCACCTACAGC-3 ′ and 5 ′ -AATCACTGT CTTGCCCCAGG-3 ′ ) ( 18 ), procollagen α 1(III) (5 ′ -TCCAACTGCTCCTACTCGCC-3 ′ and 5 ′ -GAGGGCCTG GATCTCCCTT-3 ′ ) ( 18 ), tropoelastin (5 ′ -GGTGCGGTG GTTCCTCAGCCTGG-3 ′ and 5 ′ -GGGCCTTGAGATACC Mean blood pressure (mmHg) ( 23 ), and GAPDH (5 ′ -CAGGAATTCGGT GAAGGTCGGAGTCAAGGG-3′ and 5′-AGTGGATCC GGTCATGAGTCCTCCCAGGAT-3′) (24). The PCR amplification protocol included 35 cycles of denaturing, annealing, and elongation with Taq polymerase (Cat.#R001A, TAKARA BIO Inc., Shiga, Japan).…”

Section: Cell Experimentsmentioning

confidence: 99%