A critical role for hepatic protein arginine methyltransferase 1 isoform 2 in glycemic control

Ma, Yingxu; Liu, S.; Jun, Hee-Jin; Wang, Jine; Fan, Xiaoli; Li, Guobing�; Yin, Lei; Rui, Liangyou; Weinman, Steven A.; Gong, Jianke; Wu, Jun

doi:10.1096/fj.202001061r

Cited by 11 publications

(10 citation statements)

References 45 publications

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“…Consistent with previous studies 23 , 24 , HFD treatment upregulated hepatic PRMT1 expression at mRNA and protein levels (Figure 1 A-C). Tissue fractionation analysis showed that the HFD-mediated induction of PRMT1 expression occurred predominantly in hepatocytes, but not in non-parenchymal cells (NPCs) (Figure 1 D), suggesting that hepatocytes are the key contributor to the elevated expression of PRMT1 expression in the livers of HFD-fed mice.…”

Section: Resultssupporting

confidence: 92%

“…Previous study demonstrated that fasting significantly increase hepatic PRMT1 expression and global asymmetric arginine demethylation in the livers of mice 23 . Therefore, we compared the global asymmetric arginine demethylation in the livers of HFD-fed mice with their standard chow (STC)-fed littermates.…”

Section: Resultsmentioning

confidence: 88%

“…Therefore, it is not surprising that PRMT1 regulates many cellular processes such as cell division and proliferation 22 . Recent studies reported that hepatic PRMT1 expression level was increased after 16-hr fasting in mice 23 and in obese subjects 23 , 24 . Interestingly, it was proposed that PRMT1 also regulates the lipogenesis by PGC-1α 24 .…”

Section: Introductionmentioning

confidence: 99%

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Hepatic PRMT1 ameliorates diet-induced hepatic steatosis via induction of PGC1α

Huang

et al. 2022

Theranostics

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Rationale : Over-nutrition will lead to overexpression of PRMT1 but protein hypomethylation is observed in the liver of obese subjects. The dynamic alteration of the expression and methyltransferase activity of PRMT1 in the progression of fatty liver diseases remains elusive. Methods : We used recombinant adeno-associated virus-mediated gene delivery system to manipulate the hepatic PRMT1 expression level in diet-induced obese mice to investigate the role of PRMT1 in hepatic steatosis. We further utilized a cohort of obese humans with biopsy-proven nonalcoholic fatty liver disease to support our observations in mouse model. Results : We demonstrated that knockdown of PRMT1 promoted steatosis development in liver of high-fat diet (HFD) fed mice. Over-expression of wild-type PRMT1, but not methyltransferase-defective mutant PRMT1 G80R , could alleviate diet-induced hepatic steatosis. The observation is conserved in the specimens of obese humans with biopsy-proven nonalcoholic fatty liver disease. Mechanistically, methyltransferase activity of PRMT1 was required to induce PGC-1α mRNA expression via recruitment of HNF-4α to the promoter of PGC-1α, and hence attenuated HFD-induced hepatic steatosis by enhancing PGC-1α-mediated fatty acid oxidation. Conclusions : Our results identify that activation of the PRMT1/HNF-4α/PGC-1α signaling is a potential therapeutic strategy for combating non-alcoholic fatty liver disease of obese subjects.

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Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

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Hepatic PRMT1 ameliorates diet-induced hepatic steatosis via induction of PGC1α

Huang

et al. 2022

Theranostics

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“…Consistent with a previous study, hyperglycemic conditions resulted in the reduction of β-cell proliferation. Previous studies have also demonstrated that PRMT1 plays an important role in glycemic control [38]. Furthermore, obvious diabetic phenotypes and reduced β-cell identity have been observed in pancreatic progenitor cell-specific PRMT1 knockout mice [16].…”

Section: Discussionmentioning

confidence: 96%

MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1

Lv¹,

Wang

Shen³

et al. 2022

Diabetol Metab Syndr

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Background Pancreatic β-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic β-cell dysfunction. However, the detailed mechanisms remain largely unknown. Methods RT-qPCR, western blotting, and immunofluorescence assays were used to evaluate PRMT1 and miR-574-3p levels. Cell Counting Kit-8, Advanced Dlycation End products (AGEs), Reactive Oxygen Species (ROS), and glucose-stimulated insulin secretion were assayed, and flow cytometry and RT-qPCR were performed to detect the role of PRMT1 and miR-574-3p in MIN6 cells. Luciferase reporter assays were performed to determine the interactions between PRMT1 and miR-574-3p. Results High-glucose treatment resulted in the high expression of PRMT1. PRMT1 silencing could alleviate the reduced proliferation, insulin secretion, and GLUT1 level, in addition to suppressing the induced apoptosis, and AGEs and ROS levels, under high glucose conditions. MiR-574-3p was established as an upstream regulator of PRMT1 using luciferase reporter assays. More importantly, miR-574-3p reversed the effect of PRMT1 silencing in MIN6 cells. Conclusions miR-574-3p suppresses glucose toxicity-induced pancreatic β-cell dysfunction by targeting PRMT1.

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“…PRMT1 also promotes asthma by regulating asthma-related pri-let-7i and pri-miR-423 [31]. PRMT1-v2 activated the gluconeogenic program in hepatocytes via interactions with PGC1α, a key transcriptional coactivator regulating gluconeogenesis [32]. PRMT1 is involved in the progression of lung cancer by regulating the high expression of FEN1 [33].…”

Section: Discussionmentioning

confidence: 99%

The Role of Protein Arginine Methyltransferase 1 in Gastrointestinal Cancers

Zou¹,

Shen²,

Ying³

2021

Post-Translational Modifications in Cellular Functions and Diseases

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Mammals can produce nine kinds of arginine methylation enzymes that can be divided into three types (I, II, and III) according to their catalytic activity. Arginine methyltransferase 1 (PRMT1), as the first discovered arginine methyltransferase type I, has been reported to be involved in cell signal transduction, DNA damage repair, RNA transcription and other processes. Its imbalance or abnormal expression is also involved in cancer metastasis. PRMT1 is highly expressed in gastrointestinal tumors and promotes tumor biomarkers expression, chemotherapy resistance and tumorigenicity to promote cancer progression, while downregulation of PRMT1 expression can inhibit the migration and invasion of related tumor cells or promote tumor cells apoptosis and inhibit the progression of cancer. Therefore, PRMT1 may be a cancer therapeutic target. In this paper, arginine methylase 1 expression in various types of gastrointestinal tumors, the tumorigenic mechanism and the role of PRMT1 in tumorigenesis and development were reviewed.

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A critical role for hepatic protein arginine methyltransferase 1 isoform 2 in glycemic control

Cited by 11 publications

References 45 publications

Hepatic PRMT1 ameliorates diet-induced hepatic steatosis via induction of PGC1α

Hepatic PRMT1 ameliorates diet-induced hepatic steatosis via induction of PGC1α

MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1

The Role of Protein Arginine Methyltransferase 1 in Gastrointestinal Cancers

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