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LncRNA-SNHG3 promotes neuroinflammation post-intracerebral hemorrhage by regulating the miR-106b-5p/txnip axis

MOLECULAR & CELLULAR TOXICOLOGY 2024年第4期20卷 883-894页

作者： Zhou, Fenggang Wu, Fei Wang, Xinran Yu, Shihua Tian, Wenqi Lv, Ou Harbin Med Univ Dept Neurosurg Affiliated Hosp 2 246 Xuefu Rd Harbin 150086 Heilongjiang Peoples R China Harbin Med Univ Dept Neurol Affiliated Hosp 2 246 Xuefu Rd Harbin 150086 Heilongjiang Peoples R China

BackgroundIntracerebral hemorrhage (ICH) stands as the most fatal stroke subtype, lacking any specific therapeutic approach yielding benefits for functional *** aimed to explore the involvement of long non-coding RNA small nucleolar RNA host gene 3 (lncRNA-SNHG3) in post-ICH neuroinflammation, offering a novel rationale for ICH *** tissues of ICH-induced mice exhibited upregulated levels of lncRNA-SNHG3. Inhibition of lncRNA-SNHG3 led to reduced modified neurological severity scores, diminished brain edema, and attenuated inflammatory infiltration, coupled with reduced levels of tumor necrosis factor-alpha/interleukin-1 beta. By repressing miR-106b-5p via targeted binding, lncRNA-SNHG3 facilitated the inhibition of transcriptional and protein levels of thioredoxin-interacting protein (txnip) through targeted binding to txnip mRNA. The counteraction of miR-106b-5p inhibition or the upregulation of txnip reversed the ameliorative effect of sh-SNHG3 on *** binding of lncRNA-SNHG3 to miR-106b-5p resulted in the upregulation of txnip, consequently inducing neuroinflammation and exacerbating ICH-induced damage.

关键词： Intracerebral hemorrhage lncRNA-SNHG3 miR-106b-5p txnip Neuroinflammation

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Thioredoxin-interacting protein (txnip) inhibition promotes retinal ganglion cell survival and facilitates M1-like microglial transformation via the PI3K/Akt pathway in glaucoma

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MOLECULAR MEDICINE 2024年第1期30卷 1-21页

作者： Chen, Junjue Zhong, Huimin Shen, Bingqiao Yu, Huan Zhang, Yang Han, Ruiqi Huang, Ping Huang, Shouyue Zhong, Yisheng Shanghai Jiao Tong Univ Ruijin Hosp Affiliated Dept Ophthalmol Med Sch 197 Ruijin Er Rd Shanghai 200025 Peoples R China Shanghai Jiao Tong Univ Shanghai Gen Hosp Shanghai Peoples Hosp 1 Dept OphthalmolSch Med Shanghai Peoples R China Shanghai Jiao Tong Univ Shanghai Key Lab Bone & Joint Dis Shanghai Inst Traumatol & Orthopaed Ruijin HospAffiliated Med Sch 197 Ruijin Er Rd Shanghai 200025 Peoples R China Shanghai Jiao Tong Univ Ruijin Hosp Affiliated Dept Ophthalmol Zhoushan BranchMed Sch Zhoushan Peoples R China

BackgroundGlaucoma is a group of heterogeneous neurodegenerative diseases with abnormal energy metabolism and imbalanced neuroinflammation in the retina. Thioredoxin-interacting protein (txnip) is involved in glucose and lipid metabolism, and associated with oxidative stress and inflammation, however, not known whether to be involved in glaucoma neuropathy and its underlying *** establish the chronic ocular hypertension (COH) mice model. Western blot, RT-PCR, immunofluorescence and F-VEP were used to detect neuroinflammation level, glial activation and RGCs survival in retina of wild type, txnip knockout and MCC950 treatment COH mice. Microglia high-pressure cultured model was constructed. Western blot, RT-PCR and immunofluorescence were used to investigate the proinflammatory cytokines secretion, glucose uptake and phenotype transformation in wild type, txnip knockout and overexpressed microglia combined with IL-17A treatment. Finally, we explored the possible underlying mechanisms using relevant pathway inhibitor *** this study, for the first time we reported that txnip expression was remarkably increased in experimental glaucomatous retina of chronic ocular hypertension (COH) mice, and it was mainly expressed in the ganglion cells layer (GCL). In addition, we found that ablation of txnip promoted retinal ganglion cells (RGCs) survival and alleviated visual function impairment in experimental glaucoma. Then, we explored the spatiotemporal consistency between glial activation and retinal inflammation levels in COH mice respectively with txnip-deficiency and under treatment of a thermo-containing protein domain 3 (NLRP3) inhibitor MCC950, and the results indicated that txnip probably mediated neuroinflammation in glaucomatous retina by activating microglia. Furthermore, upregulation of txnip was found in pressure-stimulated microglia, whereas silencing txnip facilitated microglial polarization trending towards M1 type and reduced

关键词： txnip Microglia Experimental glaucoma PI3K/AKT Neuroinflammation Energy metabolism

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Targeting txnip in endothelial progenitors mitigates IL-8-induced neutrophil recruitment under metabolic stress

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STEM CELL RESEARCH & THERAPY 2024年第1期15卷 225页

作者： Jolibois, Julia Domingues, Alison El Hamaoui, Divina Awaida, Raphael Berger-de-Gaillardo, Mathilde Guerin, Daniel Smadja, David M. Marquet-DeRouge, Perrine Margaill, Isabelle Rossi, Elisa Nivet-Antoine, Valerie Univ Paris Cite INSERM Innovat Therapeut Hemostase F-75006 Paris France Hop Necker Enfants Malad AP HP Lab Biochim Gen F-75015 Paris France Hop Europeen Georges Pompidou AP HP Lab Hematol F-75015 Paris France

BackgroundThis study explores the potential role of Thioredoxin-interacting protein (txnip) silencing in endothelial colony-forming cells (ECFCs) within the scope of age-related comorbidities and impaired vascular repair. We aim to elucidate the effects of txnip silencing on vasculogenic properties, paracrine secretion, and neutrophil recruitment under conditions of metabolic ***, isolated from human blood cord, were transfected with txnip siRNA and exposed to a high glucose and beta-hydroxybutyrate (BHB) medium to simulate metabolic stress. We evaluated the effects of txnip silencing on ECFCs' functional and secretory responses under these conditions. Assessments included analyses of gene and protein expression profiles, vasculogenic properties, cytokine secretion and neutrophil recruitment both in vitro and in vivo. The in vivo effects were examined using a murine model of hindlimb ischemia to observe the physiological relevance of txnip modulation under metabolic *** silencing did not mitigate the adverse effects on cell recruitment, vasculogenic properties, or senescence induced by metabolic stress in ECFCs. However, it significantly reduced IL-8 secretion and consequent neutrophil recruitment under these conditions. In a mouse model of hindlimb ischemia, endothelial deletion of txnip reduced MIP-2 secretion and prevented increased neutrophil recruitment induced by age-related *** findings suggest that targeting txnip in ECFCs may alleviate ischemic complications exacerbated by metabolic stress, offering potential clinical benefits for patients suffering from age-related comorbidities.

关键词： Endothelial progenitors Metabolic stress Age-related comorbidities txnip Cytokine secretion Neutrophils

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METTL3 Modulates txnip Expression to Affect the Activation of NLRP3 Inflammasome in Hepatic Cells Under Oxygen-Glucose Deprivation/Reperfusion Injury

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INFLAMMATION 2024年第3期47卷 1028-1040页

作者： Zhang, Yong Lv, Jianrui Bai, Jian Zhang, Xue Wu, Gang Lei, Xiaoming Li, Wei Zhang, Zhenni Xi An Jiao Tong Univ Dept Gastroenterol Affiliated Hosp 2 157 Xiwu Rd Xian 710004 Shaanxi Peoples R China Capital Med Univ Xuanwu Hosp Dept Gen Surg Beijing Peoples R China Capital Med Univ Beijing Friendship Hosp Dept Gen Practice Beijing Peoples R China

Hepatic ischemia-reperfusion (I/R) injury is still a major risk factor and unsolved problem in hepatic surgery. Methyltransferase-like 3 (METTL3), an important m(6)A-modified methylase, regulates inflammation and cellular stress response. In this study, we demonstrated the special role of METTL3 and its underlying mechanism in hepatic I/R injury. In the mouse model of hepatic I/R and in the oxygen-glucose deprivation and reoxygenation (OGD/R)-induced AML12 and NCTC 1469 cells, the expression of METTL3 was significantly upregulated. Inhibition of METTL3 in OGD/R-induced AML12 and NCTC 1469 cells both increased the cell viability, declined the cell apoptosis, and decreased the reactive oxygen species (ROS) and the release levels of interleukin-1 beta (IL-1 beta) and interleukin-18 (IL-18), diminishing NLRP3 and Caspase1-p20 expressions. Moreover, METTL3 positively modulated txnip expression in an m(6)A manner. txnip overexpression reversed the effects of METTL3 knockdown on OGD/R-induced injury in AML12 cells. Furthermore, inhibition of NLRP3 inflammasome activity contributed to the protective effects of txnip knockdown in OGD/R-induced AML12 cells. In conclusion, METTL3 knockdown alleviated OGD/R-induced hepatocyte injury, and the specific mechanism was associated with the inhibition of NLRP3 inflammasome activation, which was attributed to the reduction of txnip in an m(6)A-dependent manner.

关键词： Hepatic ischemia/reperfusion injury m(6)A modification METTL3 txnip NLRP3 inflammasome

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Knockdown of txnip alleviates gestational diabetes mellitus by activating autophagy to regulate cell proliferation and apoptosis in high glucose-treated trophoblasts

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REPRODUCTIVE BIOLOGY 2024年第1期24卷 100841-100841页

作者： Gu, Ying Cao, Minkai Chen, Yu Li, Jingyang Hu, Lingli Yang, Xiao-Jun Soochow Univ Affiliated Hosp 1 Dept Obstet & Gynecol Suzhou Peoples R China Jiangnan Univ Affiliated Womens Hosp Dept Obstet & Gynecol Wuxi Peoples R China Nanjing Med Univ Dept Obstet & Nanjing Nanjing Peoples R China Soochow Univ Affiliated Hosp 1 Dept Obstet & Gynecol Suzhou 215006 Jiangsu Peoples R China

Dysregulated thioredoxin-interacting protein (txnip) has been observed in women with gestational diabetes mellitus (GDM), but the specific role of txnip in GDM and the underlying mechanism remain unclear. HTR-8/ SVneo cells were treated with high glucose to mimic the injured trophoblasts of GDM. In vitro, txnip knockdown was performed by siRNA. RT-qPCR was performed to determine the expression of the corresponding genes. Cell proliferation and apoptosis were measured using CCK-8, EdU and Annexin V/PI assays. The autophagosome number was assessed using transmission electron microscopy. The expression of the autophagy substrate sequestosome 1 (P62) was evaluated by immunofluorescence. Autophagy-related proteins, including P62, light chain 3 (LC3)-I, and LC3-II, were analysed by Western blotting. HTR-8/Svneo cells treated with high glucose demonstrated reduced proliferation, increased apoptosis, decreased autophagosome formation and overall decreased autophagy. However, knockdown of txnip reversed the effects of HG on HTR-8/Svneo cells. However, the effect of txnip knockdown on HG-treated HTR-8/Svneo cells was inhibited by 3-methyladenine (3-MA) (widely used as an inhibitor of autophagy). We concluded that knockdown of txnip has the potential to enhance the activity of high glucose-treated human trophoblasts through autophagic activation, thereby improving pregnancy outcomes in patients with GDM.

关键词： GDM txnip Autophagy Trophoblast

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Increased level of txnip and nuclear translocation of TXN is associated with end stage renal disease and development of multiplex renal tumours

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BMC NEPHROLOGY 2024年第1期25卷 1页

作者： Beothe, Tamas Docs, Janos Kovacs, Gyula Peterfi, Lehel Peterfy Sandor Hosp Dept Urol Budapest Hungary Univ Pecs Med Sch Dept Urol Munkacsy Mihaly u 2 H-7621 Pecs Hungary Ruprecht Karls Univ Heidelberg Med Fac Heidelberg Germany

BackgroundEnd-stage and acquired cystic renal disease (ESRD/ACRD) kidneys are characterized by inflammatory remodelling and multiplex renal cell carcinomas (RCC). Eosinophilic vacuolated tumour (EVT) occurs exclusively in ACRD. The aim of this study was to identify the involvement of thioredoxin-interacting protein (txnip) and thioredoxin (TXN) in ESRD/ACRD *** of txnip and TXN was examined in histological slides of 6 ESRD and 6 ACRD kidneys, precursor lesions and associated tumours as well as of RCCs from the general population by *** txnip expression was seen in epithelial cells, myo-fibroblasts and endothelial cells and weak TXN expression in ESRD/ACRD kidneys and tumours. In ACRD specific EVT and its precursors TXN were translocated into *** impaired txnip/TXN redox homeostasis might be associated with development of multiplex cancer especially of EVT in ESRD/ACRD kidney.

关键词： End stage kidney txnip TXN Cancer Immunohistochemistry

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Astragaloside IV attenuates podocyte apoptosis via regulating txnip/NLRP3/GSDMD signaling pathway in diabetic nephropathy

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DIABETOLOGY & METABOLIC SYNDROME 2024年第1期16卷 1-16页

作者： Hu, Zhibo Zhou, Yu Gao, Cailing Liu, Junfen Pan, Congqing Guo, Jun Tianjin Med Univ Chu Hsien Mem Hosp 1 Tianjin Key Lab Metab Dis NHC Key Lab Hormones & Dev Tianjin 300134 Peoples R China Tianjin Med Univ Tianjin Inst Endocrinol Tianjin 300134 Peoples R China

ObjectivesAmong all the diabetes complications brought on by persistent inflammation is diabetic kidney disease (DKD). One essential method of the inflammatory response's programmed cell death is anthrax. One of the main causes of diabetic renal disease progression in a high-glycemic environment is the lysis of renal resident *** investigation sought to determine whether Astragaloside IV (AS-IV)'s anti-pyroptosis action provides a protective function for the kidneys. For 12 weeks, db/db mice received 40 mg/kg of AS-IV by transgastric gavage. To validate the possible in vitro mechanism, mouse podocytes were cultivated for additional *** vitro, AS-IV led to a significant reduction in blood urea nitrogen (BUN), urine albumen-to-creatinine ratio (UACR), serum creatinine (CREA), and hyperglycemia in db/db mice and lessen the pathological alterations in the kidney. Moreover, pyrin structural domain of the NLR family pyrin domain containing 3 (NLRP3), cleaved-caspase-1, gasdermin D (GSDMD), IL-18, and IL-1 beta were down-expressed and podocyte markers podocin and nphs1 were up-regulated following AS-IV intervention. By silencing GSDMD, we demonstrated in vitro that HG-stimulated podocytes undergo pyroptosis. We also discovered that AS-IV can mitigate this pyroptosis. To confirm that AS-IV prevented the NLRP3 inflammasome from activating, the NLRP3 inhibitor CY-09 was employed. It was also discovered that AS-IV prevents the expression of txnip and NLRP3 as well as their interaction. GSDMD expression was significantly downregulated following txnip-siRNA treatment, whereas GSDMD expression was upregulated in txnip overexpression cells;this upregulation could be undone with *** anti-pyroptosis effect of AS-IV via the txnip-NLRP3-GSDMD axis improves the renal function and podocyte damage of db/db mice and delays the onset of DKD, according to in vivo and in vitro experimental data.

关键词： Astragaloside IV Diabetic kidney disease Pyroptosis txnip NLRP3 inflammasome

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METTL3-mediated m6A modification of pri-miR-148a-3p affects prostate cancer progression by regulating txnip

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ENVIRONMENTAL TOXICOLOGY 2023年第10期38卷 2377-2390页

作者： Li, Guoqiang Liu, Junwen Wang, Yinhuai Liu, Hanqi Fu, Jianhan Zhao, Yuanqiao Huang, Yanqing Cent South Univ Xiangya Hosp 2 Dept Urol Changsha Peoples R China Cent South Univ Xiangya Sch Med Dept Histol & Embryol 172 Tongzipo Rd Changsha 410000 Peoples R China

ObjectiveProstate cancer (PCa) severely affects men's health worldwide. The mechanism of methyltransferase-like 3 (METTL3) in affecting PCa development by regulating miR-148a-3p expression via N6-methyladenosine (m6A) modification was investigated. MethodsMETTL3, miR-148a-3p, and thioredoxin interacting protein (txnip) levels were determined using RT-qPCR and Western blotting. The m6A modification level of miR-148a-3p was observed by Me-RIP assay. Bioinformatics website predicted miR-148a-3p and txnip levels in PCa and their correlation, and the binding site between them was verified by dual-luciferase assay. The proliferation, migration, invasion, and apoptosis of PCa cells were examined by CCK-8 assay, Transwell assay, and flow cytometry. A transplanted tumor model was established in nude mice to observe the tumor growth ability, followed by determination of txnip levels in tumor tissues by immunohistochemistry. ResultsMETTL3 interference restrained the proliferation, migration, and invasion and promoted apoptosis of PCa cells. METTL3 up-regulated miR-148a-3p by promoting the m6A modification of pri-miR-148a-3p in PCa cells. miR-148a-3p overexpression nullified the inhibitory actions of silencing METTL3 on PCa cell growth. miR-148a-3p facilitated PCa cell growth by silencing txnip. METTL3 interference inhibited tumor growth by down-regulating miR-148a-3p and up-regulating txnip. ConclusionMETTL3 promoted miR-148a-3p by mediating the m6A modification of pri-miR-148a-3p, thereby targeting txnip, interfering with METTL3 to inhibit the proliferation, migration and invasion of PCa cells, promote apoptosis, and inhibit tumor growth in nude mice.

关键词： epigenetics m6A METTL3 miR-148a-3p pri-miR-148a-3p prostate cancer txnip

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Ginsenoside Compound K Ameliorates Osteoarthritis by Inhibiting the Chondrocyte Endoplasmic Reticulum Stress-Mediated IRE1α-txnip-NLRP3 Axis and Pyroptosis

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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY 2023年第3期71卷 1499-1509页

作者： Tian, Yicheng Feng, Xinyuan Zhou, Zimo Qin, Sen Chen, Senxiang Zhao, Jihui Hou, Jianglin Liu, Da China Med Univ Dept Orthoped Shengjing Hosp Shenyang 110004 Liaoning Peoples R China

Osteoarthritis (OA) is a common joint disease, and studies have reported that the endoplasmic reticulum stress (ERS) in chondrocytes caused by the cartilage tissue damage could mediate the activation of Nod-like receptor protein 3 (NLRP3) inflammasomes through inositol-requiring enzyme 1 alpha (IRE1a) and thioredoxin interacting protein (txnip). Ginsenoside compound K (CK) has an inhibitory effect on IRE1a activation. However, the role of IRE1 alpha-txnip and its interaction with CK are still unclear. In this study, we examined the role and mechanism of action of CK in OA. We found that CK ameliorated OA and ERS in IL-1 beta-treated chondrocytes and a monoiodoacetate-induced rat OA model. The effect of CK on inflammation, pyroptosis, and ERS was blocked by the ERS inducer tunicamycin. In conclusion, CK hindered OA progression by inhibiting the ERS-IRE1atxnip-NLRP3 axis. Overall, our data indicate that CK could be useful in the treatment of OA and other chronic inflammatory diseases.

关键词： compound K osteoarthritis endoplasmic reticulum stress txnip

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Epigallocatechin-3-Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the txnip/NLRP3/IL-1β Signaling Pathway

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FOOD SCIENCE & NUTRITION 2024年第12期12卷 10800-10815页

作者： Wang, Yinghui Wang, Qimeng Wang, Mingming Wang, Xueling Liu, Qingzhen Lv, Shasha Nie, Huibin Liu, Gang Shandong Univ Multidisciplinary Innovat Ctr Nephrol Dept Nephrol Hosp 2 Jinan Shandong Peoples R China Shandong Univ Nephrol Res Inst Jinan Shandong Peoples R China Chengdu Univ TCM Chengdu Peoples Hosp 1 Dept Nephrol Integrated TCM & Western Med Hosp Chengdu Sichuan Peoples R China Shandong Univ Key Lab Reprod Endocrinol Minist Educ Jinan Shandong Peoples R China

Recent research indicates that the activation of the NLRP3 inflammasome is crucial in the development of diabetic kidney disease (DKD). Epigallocatechin-3-gallate (EGCG), the predominant catechin in green tea, has been noted for its anti-inflammatory properties in DKD. However, the specific mechanisms are not yet fully understood. In this study, our objective was to explore the effects of EGCG on podocytes and in diabetic kidney disease (DKD) mice and investigate how EGCG modulates the txnip/NLRP3/IL-1 beta signaling pathway in DKD, both in podocytes and animal models. In vitro, we co-cultured podocytes with EGCG and detected the viability, apoptosis, inflammation and the txnip/NLRP3/IL-1 beta signaling pathway. In vivo, DKD mice were given EGCG via oral gavage, followed by evaluations of renal function, inflammation, and the aforementioned signaling pathway. Our findings revealed that oxidative stress, inflammatory cytokines, and the txnip/NLRP3/IL-1 beta pathway were upregulated in podocytes exposed to high glucose (HG) and in the kidneys of DKD mice. However, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including txnip, ASC, caspase-1, and IL-1 beta, as well as the levels of ROS and inflammatory factors such as TNF-alpha, IL-6, and IL-18. Furthermore, in vivo, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage. In summary, our study suggests that EGCG mitigates inflammation in podocytes and DKD through the txnip/NLRP3/IL-1 beta signaling pathway, indicating potential benefits of EGCG or green tea in managing DKD.

关键词： diabetic kidney disease EGCG green tea inflammation NLRP3 txnip

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