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FOXO1Competes with Carbohydrate Response Element-binding Protein (ChREBP) and Inhibits Thioredoxin-interacting Protein (txnip) Transcription in Pancreatic Beta Cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2013年第32期288卷 23194-23202页

作者： Kibbe, Carly Chen, Junqin Xu, Guanlan Jing, Gu Shalev, Anath Univ Alabama Birmingham Comprehens Diabet Ctr Div Endocrinol Diabet & Metab Birmingham AL 35294 USA Univ Alabama Birmingham Dept Med Div Endocrinol Diabet & Metab Birmingham AL 35294 USA Univ Wisconsin Dept Pharmacol Madison WI 53792 USA

Thioredoxin-interacting protein (txnip) has emerged as an important factor in pancreatic beta cell biology, and tight regulation of txnip levels is necessary for beta cell survival. However, the mechanisms regulating txnip expression have only started to be elucidated. The forkhead boxO1 transcription factor (FOXO1) has been reported to up-regulate txnip expression in neurons and endothelial cells but to down-regulate txnip in liver, and the effects on beta cells have remained unknown. We now have found that FOXO1 binds to the txnip promoter in vivo in human islets and INS-1 beta cells and significantly decreases txnip expression. txnip promoter deletion analyses revealed that an E-box motif conferring carbohydrate response element-binding protein (ChREBP)-mediated, glucose-induced txnip expression is necessary and sufficient for this effect, and electromobility shift assays confirmed FOXO1 binding to this site. Moreover, FOXO1 blocked glucose-induced txnip expression and reduced glucose-induced ChREBP binding at the txnip promoter without affecting ChREBP expression or nuclear localization, suggesting that FOXO1 may compete with ChREBP for binding to the txnip promoter. In fact, a FOXO1 DNA-binding mutant (FOXO1-H215R) failed to inhibit txnip transcription, and the effects were not restricted to txnip as FOXO1 also inhibited transcription of other ChREBP target genes such as liver pyruvate kinase. Together, these results demonstrate that FOXO1 inhibits beta cell txnip transcription and suggest that FOXO1 confers this inhibition by interfering with ChREBP DNA binding at target gene promoters. Our findings thereby reveal a novel gene regulatory mechanism and a previously unappreciated cross-talk between FOXO1 and ChREBP, two major metabolic signaling pathways.

关键词： Beta Cell Diabetes FOXO Thioredoxin Transcription Regulation ChREBP txnip

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Structural basis for the regulatory role of the PPxY motifs in the thioredoxin-interacting protein txnip

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BIOCHEMICAL JOURNAL 2016年第2期473卷 179-187页

作者： Liu, Yanli Lau, Johnathan Li, Weiguo Tempel, Wolfram Li, Li Dong, Aiping Narula, Ashrut Qin, Su Min, Jinrong Cent China Normal Univ Coll Life Sci Hubei Key Lab Genet Regulat & Integrat Biol Wuhan 430079 Peoples R China Univ Toronto Struct Genom Consortium 101 Coll St Toronto ON M5G 1L7 Canada Cent China Normal Univ Coll Chem Key Lab Pesticide & Chem Biol Wuhan 430079 Peoples R China South Univ Sci & Technol China Mat Characterizat & Preparat Ctr Shenzhen 518055 Peoples R China South Univ Sci & Technol China Life Sci Res Ctr Shenzhen 518055 Peoples R China Univ Toronto Dept Physiol Med Sci Bldg Toronto ON M5S 1A8 Canada

txnip (thioredoxin-interacting protein) negatively regulates the antioxidative activity of thioredoxin and participates in pleiotropic cellular processes. Its deregulation is linked to various human diseases, including diabetes, acute myeloid leukaemia and cardiovascular diseases. The E3 ubiquitin ligase Itch (Itchy homologue) polyubiquitinates txnip to promote its degradation via the ubiquitin-proteasome pathway, and this Itch-mediated polyubiquitination of txnip is dependent on the interaction of the four WW domains of Itch with the two PPxY motifs of txnip. However, the molecular mechanism of this interaction of txnip with Itch remains elusive. In the present study, we found that each of the four WW domains of Itch exhibited different binding affinities for txnip, whereas multivalent engagement between the four WW domains of Itch and the two PPxY motifs of txnip resulted in their strong binding avidity. Our structural analyses demonstrated that the third and fourth WW domains of Itch were able to recognize both PPxY motifs of txnip simultaneously, supporting a multivalent binding mode between Itch and txnip. Interestingly, the phosphorylation status on the tyrosine residue of the PPxY motifs of txnip serves as a molecular switch in its choice of binding partners and thereby downstream biological signalling outcomes. Phosphorylation of this tyrosine residue of txnip diminished the binding capability of PPxY motifs of txnip to Itch, whereas this phosphorylation is a prerequisite to the binding activity of txnip to SHP2 [SH2 (Src homology 2) domain-containing protein tyrosine phosphatase 2] and their roles in stabilizing the phosphorylation and activation of CSK (c-Src tyrosine kinase).

关键词： Itch phosphotyroine PPxY motifs SHP2 txnip

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Role of PPAR-β/δ/miR-17/txnip pathway in neuronal apoptosis after neonatal hypoxic-ischemic injury in rats

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NEUROPHARMACOLOGY 2018年第0期140卷 150-161页

作者： Gamdzyk, Marcin Doycheva, Desislava Met Malaguit, Jay Enkhjargal, Budbazar Tang, Jiping Zhang, John H. Loma Linda Univ Sch Med Basic Sci Dept Physiol & Pharmacol Loma Linda CA 92354 USA Loma Linda Univ Sch Med Dept Anesthesiol Neurosurg & Neurol Loma Linda CA USA

Activation of peroxisome proliferator activated receptor beta/delta (PPAR-beta/delta), a nuclear receptor acting as a transcription factor, was shown to be protective in various models of neurological diseases. However, there is no information about the role of PPAR-beta/delta as well as its molecular mechanisms in neonatal hypoxia-ischemia (HI). In the present study, we hypothesized that PPAR-beta/delta agonist GW0742 can activate miR-17-5p, consequently inhibiting txnip and ASK1/p38 pathway leading to attenuation of apoptosis. Ten-day-old rat pups were subjected to right common carotid artery ligation followed by 2.5 h hypoxia. GW0742 was administered intranasally 1 and 24 h post HI. PPAR-13/8 receptor antagonist GSK3787 was administered intranasally 1 h before and 24 h after HI, antimir-17-5p and txnip CRISPR activation plasmid were administered intracerebroventricularly 24 and 48 h before HI, respectively. Brain infarct area measurement, neurological function tests, western blot, reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR), Fluoro-Jade C and immunofluorescence staining were conducted. GW0742 reduced brain infarct area, brain atrophy, apoptosis, and improved neurological function at 72 h and 4 weeks post HI. Furthermore, GW0742 treatment increased PPAR-beta/delta nuclear expression and miR-17-5p level and reduced txnip in ipsilateral hemisphere after HI, resulting in inhibition of ASK1/p38 pathway and attenuation of apoptosis. Inhibition of PPAR-13/8 receptor and miR-17-5p and activation of txnip reversed the protective effects. For the first time, we provide evidence that intranasal administration of PPAR-beta/delta agonist GW0742 attenuated neuronal apoptosis at least in part via PPAR-beta/delta/miR17/txnip pathway. GW0742 could represent a therapeutic target for treatment of neonatal hypoxic ischemic encephalopathy (HIE).

关键词： PPAR-beta/delta GW0742 HI Apoptosis miR-17 txnip

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MIR99AHG/miR-204-5p/txnip/Nrf2/ARE Signaling Pathway Decreases Glioblastoma Temozolomide Sensitivity

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NEUROTOXICITY RESEARCH 2022年第5期40卷 1152-1162页

作者： Zhou, Liang Ma, Junfeng Fudan Univ Shanghai Peoples Hosp 5 Dept Neurosurg 801 Heqing Rd Shanghai 200240 Peoples R China

Glioblastoma (GBM) is the most prevalent primary cerebral tumor in adults with high aggressiveness. Temozolomide (TMZ) is considered as the most widely used chemotherapy for GBM patients. Accumulating studies have proved that long non-coding RNAs (lncRNAs) participate in the pathogenesis of tumors. The aim of our study is to disclose the role of mir-99a-let-7c cluster host gene (MIR99AHG) in GBM. MIR99AHG expression was discovered to be elevated in GBM cells through quantitative real-time polymerase chain reaction (RT-qPCR) analysis. Loss-of-function experiments demonstrated that MIR99AHG silencing enhanced TMZ sensitivity of GBM both in vitro and in vivo. RNA pull down, RNA-binding protein immunoprecipitation (RIP), and luciferase reporter assays were implemented to unveil the underlying mechanism of MIR99AHG in GBM. The results of the mechanism assays implied that MIR99AHG interacted with microRNA-204-5p (miR-204-5p) and enhanced thioredoxin interacting protein (txnip) expression to inactivate the Nrf2/ARE signaling pathway. MIR99AHG/miR-204-5p/txnip regulatory axis was verified by rescue experiments in GBM. To summarize, MIR99AHG plays a promoting role in the TMZ resistance of GBM cells. The findings in this study might provide novel sight for the treatment for GBM.

关键词： Glioblastoma MIR99AHG miR-204-5p txnip Nrf2 ARE signaling pathway

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Disrupting CISD2 function in cancer cells primarily impacts mitochondrial labile iron levels and triggers txnip expression

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FREE RADICAL BIOLOGY AND MEDICINE 2021年 176卷 92-104页

作者： Karmi, Ola Sohn, Yang-Sung Zandalinas, Sara, I Rowland, Linda King, Skylar D. Nechushtai, Rachel Mittler, Ron Univ Missouri Sch Med Dept Surg Christopher S Bond Life Sci Ctr 1201 Rollins St Columbia MO 65201 USA Hebrew Univ Jerusalem Alexander Silberman Inst Life Sci Edmond J Safra Campus Givat Ram IL-91904 Jerusalem Israel Univ Missouri Coll Agr Food & Nat Resources Div Plant Sci & Interdisciplinary Plant Grp Christopher S Bond Life Sci Ctr 1201 Rollins St Columbia MO 65201 USA

The CISD2 (NAF-1) protein plays a key role in regulating cellular homeostasis, aging, cancer and neurodegenerative diseases. It was found to control different calcium, reactive oxygen species (ROS), and iron signaling mechanisms. However, since most studies of CISD2 to date were conducted with cells that constitutively lack, overexpress, or contain mutations in CISD2, the relationships between these different signaling processes are unclear. To address the hierarchy of signaling events occurring in cells upon CISD2 disruption, we developed an inducible system to express CISD2, or the dominant-negative H114C inhibitor of CISD2, in human breast cancer cells. Here, we report that inducible disruption of CISD2 function causes an immediate disruption in mitochondrial labile iron (mLI), and that this disruption results in enhanced mitochondrial ROS (mROS) levels. We further show that alterations in cytosolic and ER calcium levels occur only after the changes in mLI and mROS levels happen and are unrelated to them. Interestingly, disrupting CISD2 function resulted in the enhanced expression of the tumor suppressor thioredoxin-interacting protein (txnip) that was dependent on the accumulation of mLI and associated with ferroptosis activation. CISD2 could therefore regulate the expression of txnip in cancer cells, and this regulation is dependent on alterations in mLI levels.

关键词： CISD2 NAF-1 Oxidative stress Reactive oxygen species (ROS) Iron homeostasis Iron-sulfur cluster [Fe-S] Ferroptosis txnip Mitochondria Cancer

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Digitoflavone (DG) attenuates LPS-induced acute lung injury through reducing oxidative stress and inflammatory response dependent on the suppression of txnip/NLRP3 and NF-κB

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BIOMEDICINE & PHARMACOTHERAPY 2017年 94卷 712-725页

作者： Meng, Min Nanjing Med Univ Huaian Peoples Hosp 1 Dept Emergency Huaian 223300 Jiangsu Peoples R China

Acute lung injury is a severe disease with a high rate of mortality. Digitoflavone (DG) was suggested to possess bioactivities to reduce oxidative stress, inflammation and to regulate apoptosis. In our study, the normal saline, a low dose of DG (12.5 mg/kg), a medium dose of DG (25 mg/kg) and a high dose of DG (50 mg/kg) were administered to male C57BL/6 mice by gavage. And then, the mice were intratracheally injected with either normal saline or lipopolysaccharide (LPS). We found that DG ameliorated LPS-induced lung injury and platelets activation, accompanied with reduced CD41 expression and neutrophil platelet aggregates (NPAs). Further, pulmonary myeloperoxidase (MPO) activity and neutrophil infiltration in the lung tissues induced by LPS were abolished by DG dose-dependently. Additionally, LPS-triggered oxidative stress and secretion of pro-inflammatory cytokines were reduced by DG administration through suppressing thioredoxin-interacting protein (txnip) and nuclear factor-kappa B (NF kappa B) signaling pathways, and their down-streaming and up-streaming signals, including xanthine oxidase (XO), NLR family, pyrin domain-containing 3 (NLRP3), ASC, Caspase-1, as well as I kappa B kinase-alpha (IKK-alpha), and I kappa B alpha. Moreover, mitogen-activated protein kinases (MAPKs) pathway was also inactivated by DG in LPS-induced mice. The in vitro study further confirmed that DG ameliorated LPS-induced inflammation and oxidative stress, which was associated with reduction of ROS. In conclusion, our data suggested that DG treatment could be considered as a promising therapy for treating acute lung injury. (C) 2017 Published by Elsevier Masson SAS.

关键词： Acute lung injury Digitoflavone Oxidative stress Inflammation txnip NF-kappa B

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The Effect of Verapamil on txnip Gene Expression, GLP1R mRNA, FBS, HbA1c, and Lipid Profile in T2DM Patients Receiving Metformin and Sitagliptin

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DIABETES THERAPY 2021年第10期12卷 2701-2713页

作者： Malayeri, Alireza Zakerkish, Mehrnoosh Ramesh, Farrokh Galehdari, Hamid Hemmati, Ali Asghar Angali, Kambiz A. Ahvaz Jundishapur Univ Med Sci Sch Pharm Dept Pharmacol Ahvaz Iran Ahvaz Jundishapur Univ Med Sci Hlth Res Inst Dept Internal Med Diabet Res Ctr Ahvaz Iran Shahid Chamran Univ Ahvaz Dept Genet Fac Sci Ahvaz Iran Ahvaz Jundishapur Univ Med Sci Sch Pharm Med Plant Res Ctr Ahvaz Iran Ahvaz Jundishapur Univ Med Sci Sch Hlth Dept Biostat & Epidemiol Ahvaz Iran

Introduction: Type 2 diabetes mellitus (T2DM) is the most common type of diabetes. A decrease in the number of pancreatic beta cells is a pathological sign of diabetes, and to date there is no drug treatment that targets damage to these cells. Pancreatic beta cells have a weak antioxidant system and are highly sensitive to oxidative stress reactions that occur within cells. Thioredoxin interacting protein (txnip) inhibits thioredoxin, which is part of the intracellular antioxidant system, thereby accelerating oxidative stress and apoptosis of pancreatic beta cells. Verapamil is a non-dihydropyridine calcium channel blocker. The efficacy of this drug to improve beta cell survival and glucose homeostasis by inhibiting txnip expression has been demonstrated in in vitro studies. Although several retrospective studies have shown a lower incidence of T2DM with verapamil treatment, no prospective intervention studies have determined the efficacy of this drug in patients with T2DM. Methods: The aim of this randomized, double-blind, placebo-controlled study was to evaluate the efficacy and safety of oral verapamil administration in T2DM patients. In this 90-day study, the effects of verapamil on fasting blood sugar (FBS), hemoglobin A1C (HbA1c), and the lipid profile were evaluated and compared with those of the placebo. Results: There was a significant decrease in HbA1c (about 0.5%) in the verapamil group at the end of the intervention period. The effects of verapamil on txnip gene expression and glucagon-like peptide-1 receptor (GLP1R) mRNA were compared with those of the placebo (at baseline, after 15 and 30 days, and at the end of the study). During the first month of the study, decreased txnip gene expression and increased GLP1R mRNA were associated with the administration of verapamil when compared with the placebo, although the differences were not significant. Conclusion: Verapamil can lead to better control of T2DM by reducing txnip gene expression and increasing be

关键词： Type 2 diabetes Randomized controlled trials Verapamil txnip

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Diltiazem mitigates acute liver injury by targeting NFκB-txnip/NLRP3 axis in Rats: New insights beyond calcium channel blockade

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INTERNATIONAL IMMUNOPHARMACOLOGY 2024年第Pt 2期143卷 113460页

作者： Elnaghy, Fatma Shehatou, George S. G. El-Kader, Eman M. Abd Saber, Sameh Delta Univ Sci & Technol Fac Pharm Dept Pharmacol Gamasa 11152 Egypt Mansoura Univ Fac Pharm Dept Pharmacol & Toxicol Mansoura 35516 Egypt

Acute liver injury is characterized by the rapid onset of inflammation in the liver, which in turn plays a role in the development of hypertension. Additionally, hypertension increases susceptibility to liver diseases associated with inflammatory states. Recently, the antihypertensive drug diltiazem has demonstrated anti-inflammatory properties and has been shown to inhibit the expression of the thioredoxin-interacting protein (txnip), an upstream regulator of the NOD-like receptor pyrin-3 (NLRP3) inflammasome pathway. In our quest for an optimal therapeutic intervention for liver inflammatory diseases, we investigated the effects of diltiazem. Herein, we employed a multi-step approach integrating computational target prediction, network analysis, and molecular docking with experimental validation to explore potential interactions between diltiazem and txnip. Our investigations in rats with thioacetamide-induced liver injury revealed the anti-inflammatory potential of diltiazem, likely due to the suppression of the NLRP3 signaling pathway via targeting txnip. Furthermore, diltiazem suppressed the priming signal induced by nuclear factor kappa-B (NF kappa B) activation, as well as subsequent inflammasome components, including cleaved caspase-1, gasdermin D, IL-1 beta, and IL-18. Consequently, diltiazem exhibited anti-pyroptotic effects in the injured liver. Additionally, diltiazem was observed to reduce BCL-2associated X-protein (Bax) levels, increase B-Cell Lymphoma-2 (BCL2) levels, and decrease the tissue expression of cleaved caspase-3, indicating potential anti-apoptotic effects. These effects were reflected in improved liver weight-to-body weight ratio, liver histology, oxidative stress parameters, and liver function. In conclusion, diltiazem shows promise as a protective agent for liver inflammatory diseases. Further research is warranted to translate these preclinical results into effective strategies for improving liver health.

关键词： Liver inflammatory diseases Diltiazem NF kappa B txnip NLRP3 inflammasome

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AMSC-derived exosomes alleviate lipopolysaccharide/D-galactosamine-induced acute liver failure by miR-17-mediated reduction of txnip/NLRP3 inflammasome activation in macrophages

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EBIOMEDICINE 2018年 36卷 140-150页

作者： Liu, Yanning Lou, Guohua Li, Aichun Zhang, Tianbao Qi, Jinjin Ye, Dan Zheng, Min Chen, Zhi Zhejiang Univ Sch Med Affiliated Hosp 1State Key Lab Diag & Treatment Collaborat Innovat Ctr Diag & Treatment Infect Di Hangzhou Zhejiang Peoples R China Zhejiang Univ Sch Med Affiliated Hosp 1 Dept Endocrinol & Metab Hangzhou Zhejiang Peoples R China

Background: Mesenchymal stem cell (MSC)-derived exosome administration has been considered as a novel cell-free therapy for liver diseases through cell-cell communication. This study was aimed to determine the effects and mechanisms of AMSC-derived exosomes (AMSC-Exo) for acute liver failure (ALF) treatment. Methods: AMSC-Exo were intravenously administrated into the mice immediately after lipopolysaccharide and D-galactosamine (LPS/GalN)-exposure and their effects were evaluated by liver histological and scrum biochemical analysis. To elucidate its mechanisms in ALF therapy, the expression levels of miRNAs and inflammasome-related genes in macrophages were evaluated by qPCR and Western blot analysis, respectively. The exosomes from miR-17-knockdowned AMSCs (AMSC-Exo(miR-1-KD)) were used for further determine the role of miR-17 in AMSC-Exo-based therapy. Findings: AMSC-Exo administration significantly ameliorated ALF as determined by reduced serum alanine aminotransferase and aspartate aminotransferase levels and hepatic inflammasome activation. Further experiments revealed that AMSC-Exo were colocalized with hepatic macrophages and could reduce inflammatory factor secretion by suppressing inflammasome activation in macrophages. Moreover, miR-17, which can suppress NLRP3 inflammasome activation by targeting txnip, was abundant in AMSC-Exo cargo. While, the therapeutic effects of AMSC-Exo(miR-1-KD) on ALF were significantly abolished as they could not effectively suppress txnip expression and consequent inflammasome activation in vitro and in vivo. Interpretation: Exosome-shuttled miR-17 plays an essential role in AMSC-Exo therapy for ALF by targeting txnip and suppressing inflammasome activation in hepatic macrophages. AMSC-Exo-based therapy may present as a promising approach for txnip/NLRP3 inflammasome-related inflammatory liver diseases. (C) 2018 The Authors. Published by Elsevier B.V.

关键词： Mesenchymal stem cells Exosome Macrophage miR-17 txnip NLRP3 inflammasome

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Retrospective analysis of the relationship between elevated plasma levels of txnip and carotid intima-media thickness in subjects with impaired glucose tolerance and early Type 2 diabetes mellitus

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DIABETES RESEARCH AND CLINICAL PRACTICE 2015年第2期109卷 372-377页

作者： Zhao, Yongcai Li, Xinsheng Tang, Shiling CangZhou Cent Hosp Dept Endocrinol Cangzhou Peoples R China

Aims: Accelerated atherosclerosis is the major cause of mortality in diabetic patients and increased oxidative stress probably plays an important role in its development. The aim of our study was to evaluate the relationship between thioredoxin-interacting protein (txnip) as an oxidative stress parameter and carotid artery intima-media thickness (CIMT) as an indicator of atherosclerosis in patients with early-state diabetes and impaired glucose tolerance. Methods: The study was a retrospective analysis of 90 patients with impaired glucose regulation (IGR), 80 patients with early Type 2 diabetes mellitus (T2DM), and 80 subjects with normal glucose tolerance (NGT) as the control group. It was conducted at the endocrine outpatient clinic and hospital department of Cangzhou Central Hospital (Cangzhou, China) from June 2012 to Oct. 2013. Plasma txnip was measured to evaluate the level of oxidative stress. CIMT was assessed by carotid artery ultrasonography. Soluble vascular cell adhesion molecule-1 (sVCAM-1), a risk indicator for endothelial dysfunction, was also measured. Results: Compared to the NGT control, patients with IGR showed significantly higher plasma levels of txnip (P < 0.05). Compared to the IGR group, patients with T2DM also had significantly higher plasma levels of txnip (P < 0.05). CIMT was significantly higher in the subjects with abnormal glucose metabolism than in the NGT group (P < 0.05). CIMT showed positive correlations with both txnip and sVCAM-1 levels (r = 0.56 and r = 0.49, respectively, both P < 0.01). Conclusions: The present study showed that plasma levels of txnip may be a useful predictor of subclinical atherosclerosis in Type 2 diabetic patients. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

关键词： Glucose tolerance test Glucose metabolism disorders Carotid intima-media thickness Ultrasonography Type 2 diabetes mellitus txnip

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