Thioredoxin-interacting protein mediates hepatic lipogenesis and inflammation via PRMT1 and PGC-1α regulation in vitro and in vivo

Park, Min-Jung; Kim, Dong-Il; Lim, Seul-Ki; Choi, Joo-Hee; Kim, Jong-Choon; Yoon, Kyung-Chul; Lee, Jee-Bum; Lee, Jae-Hyuk; Han, Ho Jae; Choi, Inpyo; Kim, Hyoung-Chin; Park, Soo-Hyun

doi:10.1016/j.jhep.2014.06.032

Cited by 84 publications

(77 citation statements)

References 41 publications

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“…Han et al reported that PRMT6 promotes fasting-induced hepatic gluconeogenesis via CREB-regulated transcriptional coactivator 2 (CRTC2) methylation [5]. Moreover, we found that PRMT1 and PRMT3 are involved in hepatic lipogenesis [6,7]. Increasing evidence suggests that PRMTs play important roles in liver metabolism, and impaired PRMT expression or activity may induce metabolic disorders such as type II diabetes and nonalcoholic fatty liver disease (NAFLD).…”

Section: Introductionmentioning

confidence: 57%

Insulin-induced CARM1 upregulation facilitates hepatocyte proliferation

Yeom

Kim

Park

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Introductionmentioning

confidence: 57%

Insulin-induced CARM1 upregulation facilitates hepatocyte proliferation

Yeom

Kim

Park

et al. 2015

Biochemical and Biophysical Research Communications

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“…Lipopolysaccharide-challenged TBP-2 mice exhibit elevated serum TG and TC levels, liver fat deposition, and hepatorenal injury (37). TXNIP is elevated in livers of human NAFLD patients (39). In this study, TXNIP upregulation caused hepatocellular secretion of IL-1b and IL-18 as a result of NLRP3 inflammasome activation, initiating a hepatocytedriven sterile immune response on fructose exposure, and possibly driving NASH progression.…”

Section: Figmentioning

confidence: 62%

Reactive Oxygen Species-Induced TXNIP Drives Fructose-Mediated Hepatic Inflammation and Lipid Accumulation Through NLRP3 Inflammasome Activation

Zhang

Chen

et al. 2015

Antioxidants & Redox Signaling

203

144

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Aims: Increased fructose consumption predisposes the liver to nonalcoholic fatty liver disease (NAFLD), but the mechanisms are elusive. Thioredoxin-interacting protein (TXNIP) links oxidative stress to NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation and this signaling axis may be involved in fructose-induced NAFLD. Here, we explore the role of reactive oxygen species (ROS)-induced TXNIP overexpression in fructose-mediated hepatic NLRP3 inflammasome activation, inflammation, and lipid accumulation. Results: Rats were fed a 10% fructose diet for 8 weeks and treated with allopurinol and quercetin during the last 4 weeks. Five millimolars of fructose-exposed hepatocytes (primary rat hepatocytes, rat hepatic parenchymal cells [RHPCs], HLO2, HepG2) were co-incubated with antioxidants or caspase-1 inhibitor or subjected to TXNIP or NLRP3 siRNA interference. Fructose induced NLRP3 inflammasome activation and proinflammatory cytokine secretion, janus-activated kinase 2/signal transducers and activators of transcription 3-mediated inflammatory signaling, and expression alteration of lipid metabolism-related genes in cultured hepatocytes and rat livers. NLRP3 silencing and caspase-1 suppression blocked these effects in primary rat hepatocytes and RHPCs, confirming that inflammasome activation alters hepatocyte lipid metabolism. Hepatocellular ROS and TXNIP were increased in animal and cell models. TXNIP silencing blocked NLRP3 inflammasome activation, inflammation, and lipid metabolism perturbations but not ROS induction in fructoseexposed hepatocytes, whereas antioxidants addition abrogated TXNIP induction and diminished the detrimental effects in fructose-exposed hepatocytes and rat livers. Innovation and Conclusions: This study provides a novel mechanism for fructose-induced NAFLD pathogenesis by which the ROS-TXNIP pathway mediates hepatocellular NLRP3 inflammasome activation, inflammation and lipid accumulation. Antioxidant-based interventions can inhibit the ROS-TXNIP pathway. Antioxid. Redox Signal. 22, 848-870.

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Section: Skeletal Muscle Adaptations To Disusementioning

confidence: 99%

“…In addition to reduced muscle mass, skeletal muscle atrophy is characterized by decreased muscle fiber CSA and contractile protein content (85,89,91). Other changes include endothelial degradation, increased capillary density, decreased mitochondrial quantity, higher levels of intermuscular adipose tissue and connective tissue, as well as increased expression of type 2 muscle fiber types (85,86,87,89,90,91). Chronic muscle disuse also results in increased insulin resistance, decreased calcium ion concentration, degeneration of neuromuscular junctions, nerve terminal disruption, plus decreased maximal voluntary force production and lower fatigue resistance (85,88,89,91,92,93).…”

Section: Skeletal Muscle Adaptations To Disusementioning

confidence: 99%

Protein arginine methyltransferase expression, localization, and activity during disuse-induced skeletal muscle plasticity

Stouth

Manta

Ljubicic

2018

American Journal of Physiology-Cell Physiology

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Lay AbstractSkeletal muscle is a plastic tissue that is capable of adapting to various physiological demands. Previous work suggests that protein arginine methyltransferases (PRMTs) are important players in the regulation of skeletal muscle remodelling. However, their role in disuse-induced muscle plasticity is unknown. Therefore, the purpose of this study was to investigate the role of PRMTs within the context of early, upstream signaling pathways that mediate disuse-evoked muscle remodelling. We found differential responses of the PRMTs to muscle denervation, suggesting a unique sensitivity to, or regulation by, potential upstream signaling pathways. AMP-activated protein kinase (AMPK) was among the molecules that experienced a rapid change in activity following disuse. These alterations in AMPK predicted many of the modifications in PRMT biology during inactivity, suggesting that PRMTs factor into the molecular mechanisms that precede neurogenic muscle atrophy. This study expands our understanding of the role of PRMTs in regulating skeletal muscle plasticity.

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Thioredoxin-interacting protein mediates hepatic lipogenesis and inflammation via PRMT1 and PGC-1α regulation in vitro and in vivo

Cited by 84 publications

References 41 publications

Insulin-induced CARM1 upregulation facilitates hepatocyte proliferation

Insulin-induced CARM1 upregulation facilitates hepatocyte proliferation

Reactive Oxygen Species-Induced TXNIP Drives Fructose-Mediated Hepatic Inflammation and Lipid Accumulation Through NLRP3 Inflammasome Activation

Protein arginine methyltransferase expression, localization, and activity during disuse-induced skeletal muscle plasticity

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