Protein arginine methyltransferase 1 (PRMT1) represses MHC II transcription in macrophages by methylating CIITA

Fan, Zhiwen; Li, Jianfei; Li, Ping; Ye, Qing; Xu, Huihui; Wu, Xiaoyan; Xu, Yong

doi:10.1038/srep40531

Cited by 22 publications

(15 citation statements)

References 41 publications

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“…Still, as a transcription cofactor, PRMT5 has been shown to repress IL8 expression by mechanisms involving disabling SPT5-mediated transcriptional elongation [30]. PRMT1, in turn, has been implicated in the repression of inflammation by several mechanisms, namely, by preventing RelA from binding to target genes and methylation of TRAF6 [31], repressing IFNγ-induced MHC II transcription in macrophages [32], or by methylating PIAS1 and interfering with both IFNγ and α signaling [33]. Others, however, have demonstrated that PRMT1-mediated methylation of STAT1 is required for IFNα/β-induced transcription [34].…”

Section: Discussionmentioning

confidence: 99%

Transcriptional and Metabolomic Analysis of L-Arginine/Nitric Oxide Pathway in Inflammatory Bowel Disease and Its Association with Local Inflammatory and Angiogenic Response: Preliminary Findings

Krzystek−Korpacka

Fleszar

Bednarz−Misa

et al. 2020

IJMS

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L-arginine/nitric oxide pathway in Crohn's disease (CD) and ulcerative colitis (UC) is poorly investigated. The aim of current study is to quantify pathway serum metabolites in 52 CD (40 active), 48 UC (33 active), and 18 irritable bowel syndrome patients and 40 controls using mass spectrometry and at determining mRNA expression of pathway-associated enzymes in 91 bowel samples. Arginine and symmetric dimethylarginine decreased (p < 0.05) in active-CD (129 and 0.437 µM) compared to controls (157 and 0.494 µM) and active-UC (164 and 0.52 µM). Citrulline and dimethylamine increased (p < 0.05) in active-CD (68.7 and 70.9 µM) and active-UC (65.9 and 73.9 µM) compared to controls (42.7 and 50.4 µM). Compared to normal, CD-inflamed small bowel had downregulated (p < 0.05) arginase-2 by 2.4-fold and upregulated dimethylarginine dimethylaminohydrolase (DDAH)-2 (1.5-fold) and arginine N-methyltransferase (PRMT)-2 (1.6-fold). Quiescent-CD small bowel had upregulated (p < 0.05) arginase-2 (1.8-fold), DDAH1 (2.9-fold), DDAH2 (1.5-fold), PRMT1 (1.5-fold), PRMT2 (1.7-fold), and PRMT5 (1.4-fold). Pathway enzymes were upregulated in CD-inflamed/quiescent and UC-inflamed colon as compared to normal. Compared to inflamed, quiescent CD-colon had upregulated DDAH1 (5.7-fold) and ornithine decarboxylase (1.6-fold). Concluding, the pathway is deregulated in CD and UC, also in quiescent bowel, reflecting inflammation severity and angiogenic potential. Functional analysis of PRMTs and DDAHs as potential targets for therapy is warranted.

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Section: Discussionmentioning

confidence: 99%

Transcriptional and Metabolomic Analysis of L-Arginine/Nitric Oxide Pathway in Inflammatory Bowel Disease and Its Association with Local Inflammatory and Angiogenic Response: Preliminary Findings

Krzystek−Korpacka

Fleszar

Bednarz−Misa

et al. 2020

IJMS

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“…Enzymes that control histone modification, such as HMTs [137][138][139][140][141][143][144][145][146][148][149][150][151][152], HDMs [31,[154][155][156][157], HDACs [15,66,121,136,150,152,[158][159][160][161][162][163][164][165][166][167][168][169][170][171][172][173], BETs [174,175] are involved in the epigenetic regulation of M1 and M2 macrophage polarization (Table 2, Figure 1). Activation of the TLR-dependent pathway in macrophages and THP1 cells is accompanied by an increase in the expression of the H3K79 inhibitor-disruptor of telomeric silencing-1-like (Dot1l) [187].…”

Section: Histone Modificationmentioning

confidence: 99%

Transcriptional, Epigenetic and Metabolic Programming of Tumor-Associated Macrophages

Larionova

Kazakova

Patysheva

et al. 2020

Cancers

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Macrophages are key innate immune cells in the tumor microenvironment (TME) that regulate primary tumor growth, vascularization, metastatic spread and tumor response to various types of therapies. The present review highlights the mechanisms of macrophage programming in tumor microenvironments that act on the transcriptional, epigenetic and metabolic levels. We summarize the latest knowledge on the types of transcriptional factors and epigenetic enzymes that control the direction of macrophage functional polarization and their pro- and anti-tumor activities. We also focus on the major types of metabolic programs of macrophages (glycolysis and fatty acid oxidation), and their interaction with cancer cells and complex TME. We have discussed how the regulation of macrophage polarization on the transcriptional, epigenetic and metabolic levels can be used for the efficient therapeutic manipulation of macrophage functions in cancer.

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“…Alternatively, a study using IFNg-stimulated RAW264.7 cells revealed PRMT1 negatively regulates the M1 phenotype by repressing CIITA. Additionally, it was observed that PRMT1 is downregulated by IFNγ signaling [ 26 ]. Thus, PRMT1 adopts opposing roles in epigenetic regulation of M1s and M2s with its expression driving an M2 polarization.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic control of macrophage polarization: implications for targeting tumor-associated macrophages

Groot

Pienta

2018

Oncotarget

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The progression of cancer is a result of not only the growth of the malignant cells but also the behavior of other components of the tumor microenvironment (TME). Tumor-associated macrophages (TAMs) are key components of the TME that influence tumor growth and disease progression. TAMs can either inhibit or support tumor growth depending on their polarization to classically-activated macrophages (M1s) or alternatively-activated macrophages (M2s), respectively. Epigenetic regulation plays a significant role in determining this polarization and manipulating the epigenetic regulation in macrophages would provide a means for selectively targeting M2s thereby eliminating tumor-supporting TAMs while sparing tumor-inhibiting M1 TAMs. Many pharmacologic modulators of epigenetic enzymes are currently used clinically and could be repurposed for treating tumors with high TAM infiltrate. While much research involving epigenetic enzymes and their modulators has been performed in M1s, significantly less is known about the epigenetic regulation of M2s. This review highlights the field’s current knowledge of key epigenetic enzymes and their pharmacologic modulators known to influence macrophage polarization.

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Protein arginine methyltransferase 1 (PRMT1) represses MHC II transcription in macrophages by methylating CIITA

Cited by 22 publications

References 41 publications

Transcriptional and Metabolomic Analysis of L-Arginine/Nitric Oxide Pathway in Inflammatory Bowel Disease and Its Association with Local Inflammatory and Angiogenic Response: Preliminary Findings

Transcriptional and Metabolomic Analysis of L-Arginine/Nitric Oxide Pathway in Inflammatory Bowel Disease and Its Association with Local Inflammatory and Angiogenic Response: Preliminary Findings

Transcriptional, Epigenetic and Metabolic Programming of Tumor-Associated Macrophages

Epigenetic control of macrophage polarization: implications for targeting tumor-associated macrophages

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