Serum amyloid A stimulates macrophage foam cell formation via lectin-like oxidized low-density lipoprotein receptor 1 upregulation

Lee, Ha Young; Kim, Sang Doo; Baek, Suk‐Hwan; Choi, Joon Hyuk; Cho, Kyung‐Hyun; Zabel, Brian A.; Bae, Yoe‐Sik

doi:10.1016/j.bbrc.2013.02.077

Cited by 40 publications

(37 citation statements)

References 39 publications

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“…As a result, SAA binding to HDL alters its protective function against the development of atherosclerosis [6, 36]. Previous studies have reported that SAA could enhance oxidized LDL-induced foam cell formation, which plays an important role in the pathogenesis of atherosclerosis [37]. Although the epigenetic regulation of this process remains unclear, Jmjd3 expression was increased in patients with familial hypercholesterolemia (FH) compared with healthy individuals [38] (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

“…For the effect of Jmjd3 in sterile inflammation, it is reported that Jmjd3 could mediate IL-6 gene regulation in endothelial cells following spinal cord injury [44]. Previously, it was shown that up-regulation of SAA in the blood circulation could enhance the induction of foamy macrophage formation by oxLDL and thus implicates SAA as a potential causal agent in atherogenesis [37]. In this study, we showed that attenuated macrophage foam cell formation could result from dampened proinflammatory gene induction in cells with Jmjd3 silencing.…”

Section: Discussionmentioning

confidence: 99%

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Jmjd3-mediated epigenetic regulation of inflammatory cytokine gene expression in serum amyloid A-stimulated macrophages

Yan

Sun

Zhu

et al. 2014

Cellular Signalling

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Serum amyloid A (SAA), a major acute-phase protein, has potent cytokine-like activities in isolated phagocytes and synovial fibroblasts. SAA-induced proinflammatory cytokine gene expression requires transcription factors such as NF-κB; however, the associated epigenetic regulatory mechanism remains unclear. Here we report that Jmjd3, a histone H3 lysine 27 (H3K27) demethylase, is highly inducible in SAA-stimulated macrophages and plays an important role in the induction of inflammatory cytokine genes. SAA-induced Jmjd3 expression leads to reduced H3K27 trimethylation. Silencing of Jmjd3 expression significantly inhibited SAA-induced expression of proinflammatory cytokines including IL-23p19, G-CSF and TREM-1, along with up-regulation of H3K27 trimethylation levels on their promoters. Depletion of Jmjd3 expression also attenuated the release of proinflammatory cytokine genes in a peritonitis model and ameliorated neutrophilia in SAA-stimulated mice. Finally, we observed that Jmjd3 is essential for SAA-enhanced macrophage foam cell formation by oxidized LDL. Taken together, these results illustrate a Jmjd3-dependent epigenetic regulatory mechanism for proinflammatory cytokine gene expression in SAA-stimulate macrophages. This mechanism may be subject to therapeutic intervention for sterile inflammation and atherosclerosis.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Jmjd3-mediated epigenetic regulation of inflammatory cytokine gene expression in serum amyloid A-stimulated macrophages

Yan

Sun

Zhu

et al. 2014

Cellular Signalling

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“…A C C E P T E D ACCEPTED MANUSCRIPT 11 Because lymphocyte apoptosis in the spleen are markedly induced during the pathogenesis of sepsis, leading to immune paralysis in sepsis patients, we investigated whether SMFM had any effect on this process. CLP surgery caused increases in apoptosis, as detected by DNA fragmentation analysis (TUNEL assay), of splenocytes, (Fig.…”

Section: A N U S C R I P Tmentioning

confidence: 99%

“…Mouse bone marrow-derived macrophages were generated as described previously (11). Mouse bone marrow-derived macrophages were incubated with vehicle (0.1% DMSO in PBS) or SMFM (200 µg/ml) for 30 min.…”

Section: Cytokine Release From Bone Marrow-derived Macrophagesmentioning

confidence: 99%

A novel natural compound from garlic (Allium sativum L.) with therapeutic effects against experimental polymicrobial sepsis

Lee

Park

et al. 2015

Biochemical and Biophysical Research Communications

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“…When macrophages are exposed to SAA-containing HDL, they turn into foam cells in a dose-dependent manner69 as a consequence of increased uptake of LDL69 and increased uptake and hydrolysis of cholesteryl esters from SAA-containing HDL 70. Foam cells are cholesterol-loaded macrophages that are a principal component of plaques.…”

Section: Saa Protein Function In Hdlmentioning

confidence: 99%

Particle‐induced pulmonary acute phase response may be the causal link between particle inhalation and cardiovascular disease

Saber

Jacobsen

Jackson

et al. 2014

WIREs Nanomed Nanobiotechnol

134

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Inhalation of ambient and workplace particulate air pollution is associated with increased risk of cardiovascular disease. One proposed mechanism for this association is that pulmonary inflammation induces a hepatic acute phase response, which increases risk of cardiovascular disease. Induction of the acute phase response is intimately linked to risk of cardiovascular disease as shown in both epidemiological and animal studies. Indeed, blood levels of acute phase proteins, such as C-reactive protein and serum amyloid A, are independent predictors of risk of cardiovascular disease in prospective epidemiological studies. In this review, we present and review emerging evidence that inhalation of particles (e.g., air diesel exhaust particles and nanoparticles) induces a pulmonary acute phase response, and propose that this induction constitutes the causal link between particle inhalation and risk of cardiovascular disease. Increased levels of acute phase mRNA and proteins in lung tissues, bronchoalveolar lavage fluid and plasma clearly indicate pulmonary acute phase response following pulmonary deposition of different kinds of particles including diesel exhaust particles, nanoparticles, and carbon nanotubes. The pulmonary acute phase response is dose-dependent and long lasting. Conversely, the hepatic acute phase response is reduced relative to lung or entirely absent. We also provide evidence that pulmonary inflammation, as measured by neutrophil influx, is a predictor of the acute phase response and that the total surface area of deposited particles correlates with the pulmonary acute phase response. We discuss the implications of these findings in relation to occupational exposure to nanoparticles.How to cite this article: WIREs Nanomed Nanobiotechnol 2014, 6:517–531. doi: 10.1002/wnan.1279

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Serum amyloid A stimulates macrophage foam cell formation via lectin-like oxidized low-density lipoprotein receptor 1 upregulation

Cited by 40 publications

References 39 publications

Jmjd3-mediated epigenetic regulation of inflammatory cytokine gene expression in serum amyloid A-stimulated macrophages

Jmjd3-mediated epigenetic regulation of inflammatory cytokine gene expression in serum amyloid A-stimulated macrophages

A novel natural compound from garlic (Allium sativum L.) with therapeutic effects against experimental polymicrobial sepsis

Particle‐induced pulmonary acute phase response may be the causal link between particle inhalation and cardiovascular disease

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