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Polarization of rheumatoid macrophages is regulated by the CDKN2B-AS1/MIR497/txnip axis

IMMUNOLOGY LETTERS 2021年 239卷 23-31页

作者： Li, Yu Gu, Chenxi Liu, Guanlei Yu, Yang Xu, Jianzhong Hosp Zhengzhou Univ Zhengzhou Peoples R China

The polarization of macrophages plays a critical role in the pathophysiology of rheumatoid arthritis. The macrophages can have pro-inflammatory M1 polarization and various types of alternative anti-inflammatory M2 polarization. Our preliminary results showed that the CDKN2B-AS1/MIR497/txnip axis might regulate macrophages of rheumatoid arthritis patients. Therefore, we hypothesized that this axis regulated the polarization of rheumatoid macrophages. Flow cytometry was used to determine the surface polarization markers in M1 or M2 macrophages from healthy donors and rheumatoid arthritis patients. The QPCR and Western Blotting were used to compare the expression of the CDKN2B-AS1/MIR497/txnip axis in these macrophages. We Knocked down and overexpressed the axis in the macrophage cell line MD to test its roles in macrophage polarization. Compared to cells from healthy donors, cells from rheumatoid arthritis patients expressed higher levels of CD40 and CD80 and lower levels of CD16, CD163, CD206, and CD200R after polarization, they also expressed higher CDKN2B-AS1, lower MIR497, and higher txnip. In macrophages from healthy donors, there was no correlation among CDKN2B-AS1, MIR497, and txnip. But in macrophages from patients, there were significant correlations. The CDKN2B-AS1 knockdown, MIR497 mimics suppressed the M1 polarization but promoted the M2 polarization in MD cells, while the MIR497 knockdown and the txnip overexpression did the opposite. This study demonstrated that elevated CDKN2B-AS1 in macrophages promotes the M1 polarization and inhibited the M2 polarization of macrophages by the CDKN2B-AS1/ MIR497/txnip axis.

关键词： Polarization Rheumatoid Macrophages CDKN2B-AS1 MIR497 txnip

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Exosome-mediated pyroptosis of miR-93-txnip-NLRP3 leads to functional difference between M1 and M2 macrophages in sepsis-induced acute kidney injury

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 2021年第10期25卷 4786-4799页

作者： Juan, Chen-Xia Mao, Yan Cao, Qian Chen, Yan Zhou, Lan-Bo Li, Sheng Chen, Hao Chen, Jia-He Zhou, Guo-Ping Jin, Rui Nanjing Med Univ Affiliated Hosp 1 Dept Pediat Nanjing Peoples R China Nanjing Univ Chinese Med Affiliated Hosp Jiangsu Prov Hosp Chinese Med Dept Nephrol Nanjing Peoples R China Nanjing Med Univ Affiliated Geriatr Hosp Dept Nephrol Nanjing Peoples R China Nanjing Med Univ Affiliated Hosp 1 Dept Dermatol Nanjing Peoples R China Yancheng Matern & Child Hlth Care Hosp Dept Pediat Yancheng Peoples R China Nanjing Med Univ Affiliated Hosp 1 Dept Urol Nanjing Peoples R China

Sepsis is a systemic inflammatory response syndrome caused by infection, resulting in organ dysfunction. Sepsis-induced acute kidney injury (AKI) is one of the most common potential complications. Increasing reports have shown that M1 and M2 macrophages both take part in the progress of AKI by influencing the level of inflammatory factors and the cell death, including pyroptosis. However, whether M1 and M2 macrophages regulate AKI by secreting exosome remains unknown. In the present study, we isolated the exosomes from M1 and M2 macrophages and used Western blot and enzyme-linked immunosorbent assay (ELISA) to investigate the effect of M1 and M2 exosomes on cell pyroptosis. miRNA sequencing was used to identify the different miRNA in M1 and M2 exosomes. Luciferase reporter assay was used to verify the target gene of miRNA. We confirmed that exosomes excreted by macrophages regulated cell pyroptosis in vitro by using Western blot and ELISA. miRNA sequencing revealed the differentially expressed level of miRNAs in M1 and M2 exosomes, among which miR-93-5p was involved in the regulation of pyroptosis. By using bioinformatics predictions and luciferase reporter assay, we found that thioredoxin-interacting protein (txnip) was a direct target of miR-93-5p. Further in vitro and in vivo experiments indicated that exosomal miR-93-5p regulated the txnip directly to influence the pyroptosis in renal epithelial cells, which explained the functional difference between different phenotypes of macrophages. This study might provide new targets for the treatment of sepsis-induced AKI.

关键词： AKI exosomes macrophage miR‐ 93 pyroptosis txnip

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Fluorinated curcumin derivative (Shiga-Y6) modulates the level of thioredoxin-interacting protein (txnip) in a mouse model of diabetes

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2024年 694卷 149392页

作者： Aldoghachi, Asraa Faris Yanagisawa, Daijiro Arrozi, Aslina Pahrudin Bakar, Zulzikry Hafiz Abu Taguchi, Hiroyasu Ishigaki, Shinsuke Morino, Katsutaro Tooyama, Ikuo Shiga Univ Med Sci Mol Neurosci Res Ctr Otsu Shiga Japan Shiga Univ Med Sci Med Innovat Res Ctr Otsu Japan Univ Malaya Fac Med Dept Mol Med Kuala Lumpur Malaysia Shiga Univ Med Sci Inst Res Off Otsu Japan Univ Coll Dublin Syst Biol Ireland Dublin Ireland

Thioredoxin interacting protein (txnip) has emerged as a significant regulator of 8-cell mass and loss, rendering it an attractive target for treating diabetes. We previously showed that Shiga-Y6, a fluorinated curcumin derivative, inhibited txnip mRNA and protein expression in vitro, raising the question of whether the same effect could be translated in vivo. Herein, we examined the effect of Shiga-Y6 on TNXIP levels and explored its therapeutic potential in a mouse model of diabetes, Akita mice. We intraperitoneally injected Shiga-Y6 (SY6;30 mg/ kg of body weight) or vehicle into 8-week-old Akita mice for 28 consecutive days. On day 29, the mice were euthanized, following which the serum levels of glucose, insulin, and glucagon were measured using ELISA, the expression of txnip in pancreatic tissue lysates was determined using western blotting, and the level of 8-cell apoptosis was assessed using the TUNEL assay. txnip levels in the pancreatic tissue of Akita mice were significantly elevated compared with wild-type (WT) mice. Shiga-Y6 administration for 28 days significantly lowered those levels compared with Akita mice that received vehicle to a level comparable to WT mice. In immunohistochemical analysis, both a- to 8-cell ratio and the number of apoptotic 8-cells were significantly reduced in SY6-treated Akita mice, compared with vehicle-treated Akita mice. Findings from the present study suggest a potential of Shiga-Y6 as an antidiabetic agent through lowering txnip protein levels and ameliorating pancreatic 8-cells apoptosis.

关键词： Diabetes 8-cells txnip Shiga-Y6 Akita mice

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Celastrol targets the ChREBP-txnip axis to ameliorates type 2 diabetes mellitus

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PHYTOMEDICINE 2023年 110卷 154634页

作者： Zhou, Duanfang Li, Xiaoli Xiao, Xiaoqiu Wang, Gang Chen, Bo Song, Yi Liu, Xu He, Qichen Zhang, Huan Wu, Qiuya Zhang, Limei Wu, Lihong Shen, Zhengze Hassan, Moustapha Zhao, Ying Zhou, Weiying Chongqing Med Univ Coll Pharm Dept Pharmacol Chongqing Peoples R China Chongqing Key Lab Drug Metab Chongqing Peoples R China Key Lab Biochem & Mol Pharmacol Chongqing Chongqing Peoples R China Chongqing Med Univ Dept Pharm Women & Childrens Hosp Chongqing Peoples R China Chongqing Med Univ Affiliated Hosp 1 Chongqing Key Lab Translat Med Major Metab Dis Chongqing Peoples R China Chongqing Med Univ Dept Pharm Yongchuan Hosp Chongqing Peoples R China Karolinska Inst Dept Lab Med Div Biomol & Cellular Med BCM Expt Canc Med Solna Sweden Chongqing Med Univ Coll Pharm 1 Yixueyuan Rd Chongqing 400016 Peoples R China

Backgrounds: Thioredoxin-interacting protein (txnip) plays a pivotal role in regulation of blood glucose ho-meostasis and is an emerging therapeutic target in diabetes and its complications. Celastrol, a pentacyclic tri-terpene extracted from the roots of Tripterygium wilfordii Hook F, can reduce insulin resistance and improve diabetic ***: This study aimed to untangle the mechanism of celastrol in ameliorating type 2 diabetes (T2DM) and evaluate its potential benefits as an anti-diabetic ***: db/db mice was used to evaluate the hypoglycemic effect of celastrol in vivo;Enzyme-linked immu-nosorbent assay (ELISA) and 2-NBDG assay were used to detect the effect of celastrol on insulin secretion and glucose uptake in cells;Western blotting, quantitative reverse transcription PCR (RT-qPCR) and immunohisto-logical staining were used to examine effect of celastrol on the expression of txnip and the carbohydrate response element-binding protein (ChREBP). Molecular docking, cellular thermal shift assay (CETSA), drug af-finity responsive targets stability assay (DARTS) and mass spectrometry were used to test the direct binding between celastrol and ChREBP. Loss-and gain-of-function studies further confirmed the role of ChREBP and txnip in celastrol-mediated amelioration of ***: Celastrol treatment significantly reduced blood glucose level, body weight and food intake, and improved glucose tolerance in db/db mice. Moreover, celastrol promoted insulin secretion and improved glucose ho-meostasis. Mechanistically, celastrol directly bound to ChREBP, a primary transcriptional factor upregulating txnip expression. By binding to ChREBP, celastrol inhibited its nuclear translocation and promoted its pro-teasomal degradation, thereby repressing txnip transcription and ultimately ameliorating T2DM through breaking the vicious cycle of hyperglycemia deterioration and txnip ***: Celastrol ameliorates T2DM through targeting ChREBP

关键词： Celastrol ChREBP Diabetes Metabolism txnip

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Piperine mitigates aortic vasculopathy in streptozotocin-diabetic rats via targeting txnip-NLRP3 signaling

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LIFE SCIENCES 2023年第1期314卷 000-000页

作者： Amin, Fatma M. Shehatou, George S. G. Nader, Manar A. Abdelaziz, Rania R. Mansoura Univ Fac Pharm Dept Pharmacol & Toxicol Mansoura Egypt Delta Univ Sci & Technol Fac Pharm Dept Pharmacol & Biochem Gamasa City Egypt

Several in vivo and in vitro studies reported a favorable effect of piperine (PIP) on vascular function. However, the potential impacts of PIP on macrovasculopathy in streptozotocin (STZ)-diabetic rats have not yet been ***-two Sprague Dawley rats were used (n= 8/group). STZ-administered rats (50 mg/kg once, i.p) received PIP (30 mg/kg/day, orally) or its vehicle starting from day 15 till the end of the study (10 weeks). Control groups consisted of age-matched normal rats with or without PIP treatment. Metabolic and oxidative stress parameters were biochemically determined. Aortas were histologically examined. Ex vivo aortic reactivity to phenylephrine and acetylcholine was studied. Components of the txnip-NLRP3 pathway were assessed using real-time PCR, ELISA, and immunohistochemistry. Two-way ANOVA was used to compare groups. Statistical significance was set at P < *** treatment of diabetic rats significantly reduced levels of fasting glycemia, HbA1c, and serum AGEs, TGs, TC, and LDL-C compared to control diabetic group. PIP diminished aortic endothelial denudation and fibrous tissue proliferation compared to control STZ aortas. PIP lessened aortic contractility to phenylephrine and improved aortic relaxation to acetylcholine relative to untreated STZ group. PIP administration to diabetic rats elicited significant enhancements in GSH and SOD levels, eNOS expression, and total nitrate/nitrite bioavail-ability compared to untreated STZ rats. Moreover, PIP attenuated aortic contents of ROS, MDA, txnip protein and mRNA, NF-Kappa B p65 mRNA, NLRP3 mRNA, IL-1 beta protein, and caspase-3 and TNF-alpha expressions compared to untreated STZ *** conclusion, PIP might ameliorate diabetes-associated functional and structural aortic remodeling by tar-geting txnip-NLRP3 signaling.

关键词： Diabetes STZ Aorta Piperine txnip NLRP3 ROS IL-1? Caspase-3 eNOS

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txnip overexpression in mice enhances streptozotocin-induced diabetes severity

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MOLECULAR AND CELLULAR ENDOCRINOLOGY 2023年 565卷 111885页

作者： Schneider, Marlon R. Zettler, Silja Rathkolb, Birgit Dahlhoff, Maik Univ Leipzig Inst Vet Physiol Fac Vet Med Leipzig Germany LMU Munchen Inst Mol Anim Breeding & Biotechnol Gene Ctr Munich Germany Helmholtz Zentrum Munchen Inst Expt Genet German Mouse Clin Neuherberg Germany Univ Vet Med Vienna Inst vivo & vitro Models Dept Biomed Sci Vienna Austria Univ Vet Med Vienna Inst vivo & vitro Models Vet pl 1 A-1210 Vienna Austria

Thioredoxin-interacting protein (txnip) is a key player in the endocrine pancreas;it induces beta cell apoptosis, such that txnip deficiency promotes beta cell survival. To study its function in more detail, we generated transgenic mice with ubiquitous overexpression of txnip. CBAtxnip/+ mice were investigated under basal conditions and after being challenged in diet-induced obesity (DIO) and streptozotocin-induced type 1 diabetes mellitus (T1DM) models. txnip overexpression caused no effect in the DIO model, contrasting to the already reported txnip-deficient mice. However, in the T1DM background, CBAtxnip/+ animals showed significantly enhanced blood glucose and increased glucose levels in a glucose tolerance test. Finally, the beta cell mass of CBAtxnip/+ transgenic animals in the T1DM model was significantly reduced compared to control littermates. Our study demonstrates that overexpression of txnip doesn't affect blood glucose parameters under basal conditions. However, overexpression of txnip in a T1DM model enhances the severity of the disease.

关键词： txnip Diabetes mellitus Blood glucose Mouse model Diet-induced obesity Apoptosis

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Morin attenuates pyroptosis of nucleus pulposus cells and ameliorates intervertebral disc degeneration via inhibition of the txnip/NLRP3/Caspase-1/IL-1β signaling pathway

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2021年 559卷 106-112页

作者： Zhou, Yifan Chen, Zhiqian Yang, Xiao Cao, Xiankun Liang, Zhihao Ma, Hui Zhao, Jie Shanghai Jiao Tong Univ Shanghai Peoples Hosp 9 Dept Orthopaed Surg Shanghai Key Lab Orthopaed ImplantsSch Med Shanghai Peoples R China

Intervertebral disc degeneration (IDD) is a major cause of lower back pain (LBP), a condition that causes a heavy economic burden globally. The production of cytokines, including interleukin (IL)-10 and tumor necrosis factor (TNF) a, is increased in the degenerating intervertebral disc. Thioredoxin-interacting protein (txnip) participates in NLRP3 inflammasome-dependent pyroptosis in liver. Therefore, we hypothesized that txnip maypromote pyroptosis via NLRP3/Caspase-1/IL-10 signaling pathway in nucleus pulposus (NP) cell. This study examined the effects of txnip on IDD, explored the underlying mechanisms of action and find Morin which is the inhibitor of txnip can attenuates pyroptosis of nucleus pulposus cells and ameliorates intervertebral disc degeneration. Our findings indicate that txnip promote pyroptosis via NLRP3/Caspase-1/IL-10 signaling pathway in NP cell. Morin considerably inhibited the txnip/NLRP3/Caspase-1 signaling pathway in vitro. In vivo. Our data show that txnip can aggravates intervertebral disc degeneration and morin may be a useful therapeutic agent for IDD. (c) 2021 Elsevier Inc. All rights reserved.

关键词： Intervertebral disc degeneration Morin Pyroptosis txnip

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Identification of Gm15441, a txnip antisense lncRNA, as a critical regulator in liver metabolic homeostasis

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CELL AND BIOSCIENCE 2021年第1期11卷 208页

作者： Xin, Mingyang Guo, Qian Lu, Qingchun Lu, Juan Wang, Po-shun Dong, Yun Li, Tao Chen, Ye Gerhard, Glenn S. Yang, Xiao-feng Autieri, Michael Yang, Ling Temple Univ Dept Med Genet & Mol Biochem Lewis Katz Sch Med Philadelphia PA 19140 USA First Hosp Jilin Univ Dept Intens Care Unit Changchun 130021 Peoples R China Nanxishan Hosp Guangxi Zhuang Autonomous Reg Dept Endocrinol Guilin 541001 Peoples R China Shandong First Med Univ Dept Infect Dis Shandong Prov Hosp Jinan 250021 Peoples R China No Arizona Univ Dept Math & Stat Flagsta AZ 86011 USA Temple Univ Ctr Metab Dis Res Lewis Katz Sch Med Philadelphia PA 19140 USA Temple Univ Cardiovasc Res Ctr Lewis Katz Sch Med Philadelphia PA 19140 USA

Background The majority of mammalian genome is composed of non-coding regions, where numerous long non-coding RNAs (lncRNAs) are transcribed. Although lncRNAs have been identified to regulate fundamental biological processes, most of their functions remain unknown, especially in metabolic homeostasis. Analysis of our recent genome-wide screen reveals that Gm15441, a thioredoxin-interacting protein (txnip) antisense lncRNA, is the most robustly induced lncRNA in the fasting mouse liver. Antisense lncRNAs are known to regulate their sense gene expression. Given that txnip is a critical metabolic regulator of the liver, we aimed to investigate the role of Gm15441 in the regulation of txnip and liver metabolism. Methods We examined the response of Gm15441 and txnip under in vivo metabolic signals such as fasting and refeeding, and in vitro signals such as insulin and key metabolic transcription factors. We investigated the regulation of txnip expression by Gm15441 and the underlying mechanism in mouse hepatocytes. Using adenovirus-mediated liver-specific overexpression, we determined whether Gm15441 regulates txnip in the mouse liver and modulates key aspects of liver metabolism. Results We found that the expression levels of Gm15441 and txnip showed a similar response pattern to metabolic signals in vivo and in vitro, but that their functions were predicted to be opposite. Furthermore, we found that Gm15441 robustly reduced txnip protein expression in vitro through sequence-specific regulation and translational inhibition. Lastly, we confirmed the txnip inhibition by Gm15441 in vivo (mice) and found that Gm15441 liver-specific overexpression lowered plasma triglyceride and blood glucose levels and elevated plasma ketone body levels. Conclusions Our data demonstrate that Gm15441 is a potent txnip inhibitor and a critical metabolic regulator in the liver. This study reveals the therapeutic potential of Gm15441 in treating metabolic diseases.

关键词： Gm15441 Antisense lncRNA txnip Liver metabolism

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Targeting the txnip-NLRP3 interaction with PSSM1443 to suppress inflammation in sepsis-induced myocardial dysfunction

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JOURNAL OF CELLULAR PHYSIOLOGY 2021年第6期236卷 4625-4639页

作者： Wang, Linhua Zhao, Hongsheng Xu, Huifen Liu, Xiangxin Chen, Xinlong Peng, Qingyun Xiao, Mingbing Nantong Univ Dept Crit Care Med Affiliated Hosp Nantong 226001 Jiangsu Peoples R China Nantong Univ Dept Gastroenterol Affiliated Hosp Nantong 226001 Jiangsu Peoples R China Nantong Univ Res Ctr Clin Med Affiliated Hosp Nantong 226001 Jiangsu Peoples R China

Sepsis-induced myocardial dysfunction (SIMD), a deadly symptom in sepsis patients, is mainly caused by cardiovascular inflammation. However, it remains unclear how systemic inflammation triggers and aggravates cardiovascular inflammation in the pathogenesis of SIMD. This study found that proinflammatory cytokines and H2O2 concentrations were significantly induced in SIMD-mice. In particular, a microarray analysis of CD63(+) exosomes isolated from sham- and SIMD-monocytes revealed a significant induction of thioredoxin-interacting protein (txnip) and NLR family pyrin domain-containing 3 (NLRP3). We proved that oxidative stress caused the disassociation of the txnip-TRX2 (thioredoxin 2) complex and the assembly of the txnip-NLRP3 complex. In addition, this finding showed that the latter complex could be embedded into CD63(+) exosomes and traffic from monocytes to the resident heart macrophages, where it activated caspase-1 and cleaved inactive interleukin 1 beta (IL-1 beta) and IL-18. Furthermore, using an amplified luminescent proximity homogeneous assay (Alpha) with GST-txnip and His-NLRP3, we obtained a small molecule named PSSM1443 that could disrupt the txnip-NLRP3 interaction in vitro, impairing NLRP3 downstream events. Of note, after administering PSSM1443 to the SIMD-mice, we found the small molecule could significantly suppress the activation of caspase-1 and the cleavage of pro-IL-1 beta and pro-IL-18, reducing inflammation in the SIMD-mice. Collectively, our results reveal that monocyte-derived exosomes harbor the overexpressed txnip-NLRP3 complex, which traffics from circulating monocytes to local macrophages and promotes the cleavage of inactive IL-1 beta and IL-18 in the macrophages, aggravating cardiovascular inflammation. PSSM1443 functions as an inhibitor of the txnip-NLRP3 complex and its administration can decrease inflammation in SIMD-mice.

关键词： exosome inflammation NLRP3 PSSM1443 SIMD txnip

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MEBT/MEBO通过调控txnip/NLRP3/Caspase-1信号通路促进糖尿病创面愈合

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海南医学院学报 2024年第24期30卷 1848-1858页

作者：姚明哲竺仕林李文武杨雅量葛星月唐乾利右江民族医学院研究生院广西百色533000 右江民族医学院附属医院生命科学与临床医学研究中心广西百色533000 广西中医药大学/广西中医药科学实验中心广西南宁530200

目的:探讨湿润暴露疗法/湿润烧伤膏(moist exposed burn therapy/moist exposed burn ointment,MEBT/MEBO)对糖尿病创面中txnip/NLRP3/Caspase-1信号通路表达的影响。方法:将48只Wistar雄性大鼠随机平均分为对照组、模型组、美宝组和贝复新组。其中对照组构建急性创面模型,其余组构建糖尿病创面模型。随后美宝组和贝复新组分别采用湿润烧伤膏和重组牛碱性成纤维生长因子进行换药,对照组及模型组采取生理盐水进行换药。通过H&E染色、免疫荧光法及实时荧光定量PCR检测观察各组创面第3、7、14天愈合情况及txnip、NLRP3及Caspase-1表达情况。结果:(1)治疗第3天,对照组创面愈合率高于模型组,且具有统计学差异性(P<0.05);治疗第7、14天,对照组、美宝组和贝复新组创面愈合率高于模型组(P<0.05)。(2)治疗第3、7、14天,对照组、美宝组和贝复新组的txnip、NLRP3表达量低于模型组(P<0.05):治疗第3、7、14天,对照组和美宝组的Caspase-1表达量低于模型组(P<0.05)。结论:MEBT/MEBO可通过抑制txnip/NLRP3/Caspase-1通路表达,减轻糖尿病创面的炎症反应,从而促进糖尿病创面的愈合。

关键词：湿润暴露疗法/湿润烧伤膏(MEBT/MEBO) 糖尿病创面 txnip NLRP3 Caspase-1

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