Data on TREM-1 activation destabilizing carotid plaques

Rao, Velidi H.; Rai, Vikrant; Stoupa, Samantha; Subramanian, Saravanan; Agrawal, Devendra K.

doi:10.1016/j.dib.2016.05.047

Cited by 21 publications

(16 citation statements)

References 3 publications

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“…However, inhibition of COX-2 fails to completely suppress RASF-induced TREM-1 expression in monocytes, which also suggests that the endogenous PGE 2 -mediated pathway seems to be one of the mechanisms and other unknown factors and pathways might also participate in the upregulation of TREM-1 expression in synovial monocytes. Other researchers report that besides PGE 2 , soluble factors such as TGF-β [49], TNF-α [50, 51], and monosodium urate monohydrate [52] can also induce TREM-1 expression, and most of these are also produced by RASF. Therefore, more in-depth studies are needed to elucidate the mechanism by which RASF regulate TREM-1 in synovial monocytes.…”

Section: Discussionmentioning

confidence: 99%

Rheumatoid arthritis synovial fibroblasts promote TREM-1 expression in monocytes via COX-2/PGE2 pathway

Peng

Huang

et al. 2019

Arthritis Res Ther

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Background Triggering receptor expressed on myeloid cells-1 (TREM-1) is inducible on monocyte/macrophages and neutrophils and amplifies the inflammatory response. The aim of this study was to determine whether rheumatoid arthritis synovial fibroblasts (RASF) promote the expression of TREM-1 in monocytes and its potential regulatory mechanism. Methods Synovial fluid and paired peripheral blood from rheumatoid arthritis (RA) patients were analyzed using flow cytometry. Expression of TREM-1 in monocytes was detected after co-culture with RASF, with or without pre-treatment with toll-like receptor (TLR) ligands. Whether RASF-regulated TREM-1 level in monocytes require direct cell contact or soluble factors was evaluated by transwell experiment. COX-2 expression and PGE 2 secretion in RASF were determined by quantitative PCR (qPCR) and ELISA. RASF, with and without TLR ligand stimulation, were treated with COX-2 inhibitors, COX-2 siRNA (siCOX-2) or EP1–4 antagonists, and the resulting TREM-1 level in CD14 + monocytes was measured using flow cytometry. Results TREM-1 was highly expressed in CD14 + cells from peripheral blood and especially synovial fluid from RA patients. The expression of TREM-1 in monocytes was increased by co-culture with RASF. TLR-ligand-activated RASF further elevated TREM-1 level. Transwell assay indicated that soluble factors played a key role in RASF-promoted expression of TREM-1 in monocytes. RASF, with or without stimulation by TLR ligands, increased secretion of PGE 2 in a cyclooxygenase (COX)-2-dependent manner. PGE 2 enhanced the increase in TREM-1 level in monocytes. Finally, studies using COX-2 inhibitors, COX-2 siRNA (siCOX-2) and EP1–4 antagonists, showed that RASF promotion of TREM-1 expression in monocytes was mediated by COX-2/PGE 2 /EP2,4 signaling. Conclusions Our data is the first report to reveal the critical role of RASF in upregulating TREM-1 expression in monocytes, which indicates that TREM-1 might be a novel target for RA therapy. Electronic supplementary material The online version of this article (10.1186/s13075-019-1954-3) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Rheumatoid arthritis synovial fibroblasts promote TREM-1 expression in monocytes via COX-2/PGE2 pathway

Peng

Huang

et al. 2019

Arthritis Res Ther

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“…Since increased inflammation renders the stable plaque unstable; these mediators of inflammation may play a potential role in vulnerability of atherosclerotic plaque. The role of TREM-1 and TLRs involving NF-κB and pro-inflammatory cytokines TNF-α in the pathogenesis of unstable plaque has been documented (Gargiulo et al 2015;Rai et al 2016;Rao et al 2016a;2016b).…”

Section: Introductionmentioning

confidence: 99%

The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques

Rai

Agrawal

2017

Can. J. Physiol. Pharmacol.

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“…In atherosclerosis, the role of TREM-1 is found to be in chronic inflammation, leading to macrophages, leukocyte apoptosis, and necrosis, which contribute to fatty streak buildups [ 57 , 58 ]. It has also been found to induce plaque vulnerability by TREM-1 expression of the vascular smooth muscle cells (VSMCs) and dendritic cells [ 59 , 60 ].…”

Section: Trem-1 In Cardiovascular Diseasesmentioning

confidence: 99%

TREM-1; Is It a Pivotal Target for Cardiovascular Diseases?

Kouassi

Gunasekar

Agrawal

et al. 2018

JCDD

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Cardiovascular diseases (CVDs) are as menacing as ever and still continue to kill adults worldwide, notwithstanding tremendous efforts to decrease their consequent mortality and morbidity. Lately, a growing body of research indicated that inflammation plays a pivotal role in the pathogenesis and complications of CVDs. A receptor of the immunoglobulin superfamily, triggering receptors expressed on myeloid cells-1 (TREM-1) was shown to induce and amplify the inflammation in both acute and chronic disease’ pathogenesis and progression, which hence makes it one of the most important complication factors of CVDs. Thus, studies endeavored to investigate the role played by TREM-1 in CVDs with respect to their etiologies, complications, and possible therapeutics. We examined here, for the first time, the most relevant studies regarding TREM-1 involvement in CVDs. We critically analyzed and summarized our findings and made some suggestions for furtherance of the investigations with the aim to utilize TREM-1 and its pathways for diagnostic, management, and prognosis of CVDs. Overall, TREM-1 was found to be involved in the pathogenesis of acute and chronic cardiovascular conditions, such as acute myocardial infarction (AMI) and atherosclerosis. Although most therapeutic approaches are yet to be elucidated, our present research outcome displays a promising future to utilizing the TREM-1 pathway as a potential target for understanding and managing CVDs.

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Data on TREM-1 activation destabilizing carotid plaques

Cited by 21 publications

References 3 publications

Rheumatoid arthritis synovial fibroblasts promote TREM-1 expression in monocytes via COX-2/PGE2 pathway

Rheumatoid arthritis synovial fibroblasts promote TREM-1 expression in monocytes via COX-2/PGE2 pathway

The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques

TREM-1; Is It a Pivotal Target for Cardiovascular Diseases?

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