Curcumin mediated epigenetic modulation inhibits TREM-1 expression in response to lipopolysaccharide

Yuan, Zhujun; Syed, Mansoor Ali; Panchal, Dipti; Rogers, Daniel A.; Joo, Myungsoo; Sadikot, Ruxana T.

doi:10.1016/j.biocel.2012.08.001

Cited by 60 publications

(56 citation statements)

References 49 publications

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“…Following ligation it associates with a signal transduction molecule, DAP12, triggering that initiates the secretion of inflammatory cytokines. TREM-1 has emerged as an important amplifier of TLR-in- duced inflammatory responses activating transcription factors that regulate the expression of proinflammatory cytokines and chemokines (14,16). This study provides yet another mechanism by which TREM-1 can perpetuate inflammation by inhibiting apoptosis of macrophage by activating the key anti-apoptotic proteins of the Bcl-2 family.…”

Section: Discussionmentioning

confidence: 87%

“…Blockade of TREM-1 has been shown to improve survival in animal models of infection and sepsis (12)(13)(14). We have shown that the functional consequences of TREM-1 silencing in macrophages include an altered availability of key signaling (CD14, IB␣, and MyD88), and effector molecules (MCP-1, IL-1␤, and IL-6) downstream of TLR activation.…”

mentioning

confidence: 99%

“…Furthermore, the presence of TLRs is necessary for the expression of TREM-1 in response to specific TLR ligands (15)(16)(17). These receptors have thus emerged as potent amplifiers of TLR-initiated inflammatory responses (14,16,18). Recent studies have shown that TREM-1 is highly expressed in tumor-associated tissue macrophages in colon, hepatocellular, and lung carcinoma (19 -22).…”

mentioning

confidence: 99%

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Triggering Receptor Expressed on Myeloid Cells 1 (TREM-1)-mediated Bcl-2 Induction Prolongs Macrophage Survival

Yuan

Syed

Panchal

et al. 2014

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 87%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Triggering Receptor Expressed on Myeloid Cells 1 (TREM-1)-mediated Bcl-2 Induction Prolongs Macrophage Survival

Yuan

Syed

Panchal

et al. 2014

Journal of Biological Chemistry

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“…The study revealed that curcumin possesses HDAC inhibition potential with an IC 50 of 115 μM. Hypoacetylation of histone 3 and 4, at lysine residue, was done by curcumin in TREM-1 promotor region that modulate TREM-1 gene expression (Yuan et al 2012). Chen et al reported down-regulation of HDAC-1, HDAC-3, HDAC-8 protein and up-regulation of histone H4 expression regulates Raji cell proliferation and apoptosis (Chen et al 2007).…”

Section: Epigenetic Impact Of Curcuminmentioning

confidence: 99%

Epigenetic impact of curcumin on stroke prevention

et al. 2014

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The epigenetic impact of curcumin in stroke and neurodegenerative disorders is curiosity-arousing. It is derived from Curcuma longa (spice), possesses anti-oxidative, anti-inflammatory, anti-lipidemic, neuro-protective and recently shown to exhibit epigenetic modulatory properties. Epigenetic studies include DNA methylation, histone modifications and RNA-based mechanisms which regulate gene expression without altering nucleotide sequences. Curcumin has been shown to affect cancer by altering epigenetic changes but its role as an epigenetic agent in cerebral stroke has not been much explored. Although curcumin possesses remarkable medicinal properties, the bioavailability of curcumin has limited its success in epigenetic studies and clinical trials. The present review is therefore designed to look into epigenetic mechanisms that could be induced with curcumin during stroke, along with its molecular designing with different moieties that may increase its bioavailability. Curcumin has been shown to be encapsulated in exosomes, nano-vesicles (<200 nm), thereby showing its therapeutic effects in brain diseases. Curcumin delivered through nanoparticles has been shown to be neuroregenerative but the use of nanoparticles in brain has limitations. Hence, curcumin-encapsulated exosomes along with curcumin-primed exosomes (exosomes released by curcumin-treated cells) are much needed to be explored to broadly look into their use as a novel therapy for stroke.

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“…The TREM gene cluster is located on human chromosome 6p21 and mouse chromosome 17C3 [16] [17]. TREM-1 was the first TREM identified and initial studies established TREM-1 as an amplifier of the systemic inflammatory response syndrome and sepsis [18] [19] [17] [20]. The precise ligand for TREM-1 is unknown however we and others have shown that bacterial and viral products [21] [19] induce expression of TREM-1.…”

Section: Introductionmentioning

confidence: 99%

TREM-1 Is Induced in Tumor Associated Macrophages by Cyclo-Oxygenase Pathway in Human Non-Small Cell Lung Cancer

et al. 2014

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It is increasingly recognized that the tumor microenvironment plays a critical role in the initiation and progression of lung cancer. In particular interaction of cancer cells, macrophages, and inflammatory response in the tumor microenvironment has been shown to facilitate cancer cell invasion and metastasis. The specific molecular pathways in macrophages that immunoedit tumor growth are not well defined. Triggering receptor expressed on myeloid cells 1 (TREM-1) is a member of the super immunoglobulin family expressed on a select group of myeloid cells mainly monocyte/macrophages. Recent studies suggest that expression of TREM-1 in tumors may predict cancer aggressiveness and disease outcomes in liver and lung cancer however the mechanism of TREM-1 expression in the setting of cancer is not defined. In this study we demonstrate that tumor tissue from patients with non-small cell lung cancer show an increased expression of TREM-1 and PGE2. Immunohistochemistry and immunofluorescence confirmed that the expression of TREM-1 was selectively seen in CD68 positive macrophages. By employing an in vitro model we confirmed that expression of TREM-1 is increased in macrophages that are co-cultured with human lung cancer cells. Studies with COX-2 inhibitors and siCOX-2 showed that expression of TREM-1 in macrophages in tumor microenvironment is dependent on COX-2 signaling. These studies for the first time define a link between tumor COX-2 induction, PGE2 production and expression of TREM-1 in macrophages in tumor microenvironment and suggest that TREM-1 might be a novel target for tumor immunomodulation.

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Curcumin mediated epigenetic modulation inhibits TREM-1 expression in response to lipopolysaccharide

Cited by 60 publications

References 49 publications

Triggering Receptor Expressed on Myeloid Cells 1 (TREM-1)-mediated Bcl-2 Induction Prolongs Macrophage Survival

Triggering Receptor Expressed on Myeloid Cells 1 (TREM-1)-mediated Bcl-2 Induction Prolongs Macrophage Survival

Epigenetic impact of curcumin on stroke prevention

TREM-1 Is Induced in Tumor Associated Macrophages by Cyclo-Oxygenase Pathway in Human Non-Small Cell Lung Cancer

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