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YAP/miR-524-5p axis negatively regulates txnip expression to promote chondrosarcoma cell growth

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2022年 590卷 20-26页

作者： Liu, Ri-Xu Tang, Wang Zheng, Bo-Yuan Yang, Yong Li, Zhen-Yan Gui, Tao Zhang, Huan-Tian Liu, Ning Zha, Zhen-Gang Li, Jing-Xiang Jinan Univ Affiliated Hosp 1 Ctr Joint Surg & Sports Med Guangzhou 510630 Peoples R China Jinan Univ Inst Orthoped Dis & Bone Guangzhou 510630 Peoples R China Jinan Univ Joint Dis Inst Guangdong Hong Kong Macao Greater Guangzhou 510630 Peoples R China Jinan Univ Dept Joint Surg Affiliated Shunde Hosp Foshan 528305 Peoples R China Southern Med Univ NanFang Hosp Guangzhou 510515 Peoples R China

Chondrosarcoma (CHS) is the second most common bone malignant tumor and currently has limited treatment options. We have recently demonstrated that thioredoxin interacting protein (txnip) plays a crucial role in the oncogenesis of bone sarcoma, yet its implication in CHS is underdetermined. In the present study, we first found that knockdown of txnip promotes the proliferation of CHS cell largely through increasing their glycolytic metabolism, which is well-known as Warburg effect for providing energy. Consistent with our previous report that YAP is fundamental for CHS cell growth, herein we revealed that YAP functioned as an upstream molecule of txnip, and that YAP negatively regulated txnip mRNA and protein expression both in vitro and in vivo. Mechanistically, although knockdown of YAP upregulated both the nuclear and cytoplasmic txnip expression, we did not observe any obvious interaction between YAP and txnip;instead, miRNA-524-5p was demonstrated to be required for YAP regulated txnip expression and thus controlling CHS cell growth. Together, our study reveals that txnip is a tumor suppressor in terms of CHS, and that the YAP/miRNA-524-5p/txnip signaling axis may provide a novel clue for CHS targeted therapy. (c) 2021 Elsevier Inc. All rights reserved.

关键词： Chondrosarcoma Glycolysis txnip YAP miR-524-5p

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Melatonin alleviates lead-induced intestinal epithelial cell pyroptosis in the common carps (Cyprinus carpio) via miR-17-5p/txnip axis

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FISH & SHELLFISH IMMUNOLOGY 2022年 131卷 127-136页

作者： Miao, Zhiying Miao, Zhiruo Teng, Xiaohua Xu, Shiwen Northeast Agr Univ Coll Life Sci Harbin 150030 Peoples R China Northeast Agr Univ Coll Anim Sci & Technol Harbin 150030 Peoples R China Northeast Agr Univ Coll Vet Med Harbin 150030 Peoples R China Northeast Agr Univ Coll Vet Med Key Lab Prov Educ Dept Heilongjiang Common Anim D Harbin 150030 Peoples R China

Lead (Pb) has been concerned as one of the most severe hazardous contaminants, because it can cause pyroptosis in multiple tissues of mammals and birds. Melatonin (Mel) has attracted much interest for its role in governing intestinal injury via microRNAs (miRNAs). To explore the effect of Mel on Pb exposure-induced intestinal epithelial cell pyroptosis in common carps by regulating miR-17-5p/txnip axis, the Pb exposure and Pb-Mel treated models were constructed in vivo. The results elucidated that the suppressed expression of miR-17-5p and intensified level of txnip were primarily detected in Pb-exposed gut tissues, and both abolished with Mel addition, along with downregulated Pb-mediated elevated expression of NLRP3, CASP1, IL113 and GSDMD. Additionally, the targeting relationship between miR-17-5p and txnip were demonstrated by dual-luciferase reporter assay, and on this basis, miR-17-5p NC, mimic and inhibitor cell models were established. Thereby, Thereby, the expression of txnip in the miR-17-5p mimic groups was significant lower in the Pb-exposure but still elevated than the Control group, and the expression of NLRP3 and NLRP3-dependent pyrotposis-related genes performed consistent alterations. Noticeably, the expression of txnip suppressed with Mel addition even in the miR-17-5p inhibitor cell model, resulting in the inactivation of NLRP3 inflammasome-dependent pyrop-tosis. Overall, we draw the conclusion as Mel attenuates Pb-induced intestinal epithelial cell pyroptosis via miR-17-5p/txnip axis. The present study provides a novel perspective for toxicological mechanism of Pb, and new insights for the detoxification mechanism of Mel.

关键词： Lead Melatonin Common carps Intestine Pyroptosis MiR-17-5p txnip

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Salidroside Alleviates Chronic Constriction Injury-Induced Neuropathic Pain and Inhibits of txnip/NLRP3 Pathway

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NEUROCHEMICAL RESEARCH 2022年第2期47卷 493-502页

作者： Hu, Tingting Sun, Qingyu Gou, Yu Zhang, Yurui Ding, Yumeng Ma, Yiran Liu, Jing Chen, Wen Lan, Ting Wang, Peipei Li, Qian Yang, Fei Capital Med Univ Dept Neurobiol Sch Basic Med Sci Adv Innovat Ctr Human Brain ProtectBeijing Key L 10 You An Men Wai Xi Tou Tiao Beijing 100069 Peoples R China Capital Med Univ Beijing Key Lab Neural Regenerat & Repair Adv Innovat Ctr Human Brain Protect Dept Biochem & Mol BiolSch Basic Med Sci Beijing Peoples R China Tianjin Univ Tianjin Hosp Dept Orthopaed Surg Tianjin Peoples R China

Neuropathic pain is one of the most common conditions requiring treatment worldwide. Salidroside (SAL), a phenylpropanoid glucoside extracted from Rhodiola, has been suggested to produce an analgesic effect in chronic pain. However, whether SAL could alleviate pain hypersensitivity after peripheral nerve injury and its mode of action remains unclear. Several studies suggest that activation of the spinal NOD-like receptor protein 3 (NLRP3) inflammasome and its related proteins contribute to neuropathic pain's pathogenesis. This study investigates the time course of activation of spinal NLRP3 inflammasome axis in the development of neuropathic pain and also whether SAL could be an effective treatment for this type of pain by modulating NLRP3 inflammasome. In the chronic constriction injury (CCI) mice model, spinal NLRP3 inflammasome-related proteins and txnip, the mediator of NLRP3, were upregulated from the 14th to the 28th day after injury. The txnip and NLRP3 inflammasome-related proteins were mainly present in neurons and microglial cells in the spinal dorsal horn after CCI. Intraperitoneal injection of SAL at 200 mg/kg for 14 consecutive days starting from the 7th day of CCI injury could ameliorate mechanical and thermal hypersensitivity in the CCI model. Moreover, SAL inhibited the activation of the txnip/NLRP3 inflammasome axis and mitigated the neuronal loss of spinal dorsal horn induced by nerve injury. These results indicate that SAL could produce analgesic and neuroprotective effects in the CCI model of neuropathic pain.

关键词： Salidroside NLRP3 inflammasome Neuropathic pain txnip Spinal cord

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Ceramide induces pyroptosis through txnip/NLRP3/GSDMD pathway in HUVECs

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BMC MOLECULAR AND CELL BIOLOGY 2022年第1期23卷 54页

作者： Liu, Fangfang Zhang, Yangyang Shi, Yining Xiong, Kai Wang, Fugui Yang, Jin Anhui Med Univ Affiliated Hosp 2 Dept Resp & Crit Care Med Hefei 230601 Anhui Peoples R China Chest Hosp Anhui Prov Dept Resp & Crit Care Med Hefei Anhui Peoples R China Anhui Med Univ Affiliated Hosp 2 Dept Emergency Med Hefei Anhui Peoples R China Anhui Med Univ Affiliated Hosp 2 Inst Resp Dis Hefei 230601 Anhui Peoples R China

Background: Pyroptosis of endothelial cells is a new cause of endothelial dysfunction in multiple diseases. Ceramide acts as a potential bioactive mediator of inflammation and increases vascular endothelial permeability in many diseases, whether it can aggravate vascular endothelial injury by inducing cell pyroptosis remains unknown. This study was established to explore the effects of C8-ceramide (C8-Cer) on human umbilical vein vascular endothelial cells (HUVECs) and its possible underlying mechanism. Methods: HUVECs were exposed to various concentrations of C8-Cer for 12 h, 24 h, 48 h. The cell survival rate was measured using the cell counting kit-8 assay. Western blotting and Real-time polymerase chain reaction (RT-PCR) were used to detect the pyroptosis-releated protein and mRNA expressions, respectively. Caspase-1 activity assay was used to detect caspase-1 activity. Hoechst 33342/propidium iodide double staining and flow cytometry were adopted to measure positive staining of cells. Lactate dehydrogenase release assay and enzyme-linked immunosorbent assay were adopted to measure leakage of cellular contents. FITC method was used to detect the permeability of endothelial cells. ROS fluorescence intensity were detected by flow cytometry. Results: The viability of HUVECs decreased gradually with the increase in ceramide concentration and time. Ceramide upregulated the expression of thioredoxin interacting protein (txnip), NLRP3, GSDMD, GSDMD-NT, caspase-1 and Casp1 p20 at the protein and mRNA level in a dose-dependent manner. It also enhanced the PI uptake in HUVECs and upregulated caspase-1 activity. Moreover, it promoted the release of lactate dehydrogenase, interleukin-1 beta, and interleukin-18. Meanwhile, we found that ceramide led to increased vascular permeability. The inhibitor of NLRP3 inflammasome assembly, MCC950, was able to disrupt the aforementioned positive loop, thus alleviating vascular endothelial cell damage. Interestingly, inhibition of txnip

关键词： Ceramide Endothelial cell Cell pyroptosis txnip NLRP3 GSDMD signalling pathway Vascular endothelial cell

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miR-223 Enhances the Neuroprotection of Estradiol Against Oxidative Stress Injury by Inhibiting the FOXO3/txnip Axis

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NEUROCHEMICAL RESEARCH 2022年第7期47卷 1865-1877页

作者： Pan, Qiong Ma, Jiezhi Guo, Ke Cent South Univ Dept Obstet & Gynecol Xiangya Hosp 3 Changsha 410013 Peoples R China Cent South Univ Dept Neurol Xiangya Hosp 3 Changsha 410013 Peoples R China

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by complex pathogenesis, of which oxidative stress has long been regarded as a major mechanism. Previously, the protective effects of estradiol on SH-SY5Y cells against A beta 42-induced injuries were demonstrated. In this study, the protection of SH-SY5Y cells by estradiol from H2O2-caused oxidative stress injury and Alzheimer's mice was further confirmed. H2O2 downregulated, whereas estradiol upregulated miR-223 expression. miR-223 overexpression promoted cell viability, inhibited cell apoptosis, reduced ROS levels, enhanced Superoxide Dismutase (SOD) activity, and decreased malondialdehyde (MDA) content. However, miR-223 inhibition exerted opposite effects. miR-223 directly targeted forkhead box O3 (FOXO3) and inhibited FOXO3 expression. H2O2 increased, whereas estradiol decreased thioredoxin interacting protein (txnip) levels;FOXO3 positively regulated txnip protein levels. In SH-SY5Y cells, FOXO3 overexpression increased, whereas FOXO3 knockdown reduced the cell apoptosis and ROS levels. FOXO3 bound to txnip promoter region and activated txnip transcription, whereas the activation could be partially inhibited by estradiol. Collectively, the FOXO3/txnip axis is downstream of miR-223. miR-223 enhances the neuroprotection of estradiol against oxidative stress injury through the FOXO3/txnip axis.

关键词： Neuroprotection Estradiol miR-223 FOXO3 txnip

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Antidiabetic effects of quercetin and liraglutide combination through modulation of txnip/IRS-1/PI3K pathway

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CELL BIOCHEMISTRY AND FUNCTION 2022年第1期40卷 90-102页

作者： Eraky, Salma M. Ramadan, Nehal M. El-Magd, Nada F. Abo Mansoura Univ Fac Pharm Dept Biochem Mansoura 35516 Egypt Mansoura Univ Fac Med Clin Pharmacol Dept Mansoura Egypt

The study was designed to assess the possible augmented antidiabetic effects of combining quercetin and liraglutide in a type 1 diabetes model, with emphasis on the contribution of hepatic thioredoxin interacting protein (txnip)/insulin receptor substrate 1 (IRS-1)/phosphatidyl inositol-3 kinase (PI3K) pathway. The wound-healing effects were also examined. Diabetes was induced by a single i.p STZ injection (55 mg/kg). Diabetic rats were treated with either quercetin (100 mg/kg/day, orally) or liraglutide (0.3 mg/kg/twice daily, S.C.) or their combination. Drugs were also applied topically on the wound. Blood glucose levels, serum albumin, total protein, total cholesterol and triglycerides were measured. Histopathological examination of the liver, pancreas and skin tissues was performed using haematoxylin and eosin staining. The hepatic malondialdehyde level was measured spectrophotometrically. Hepatic txnip and PI3K levels were measured by enzyme-linked immunsorbent assay (ELISA). Tissue expression of IRS-1 and phospho-IRS-1 (Ser 616) was assessed by immunohistochemistry. Quercetin, liraglutide and their combination effectively decreased blood glucose levels, improved lipid profile, upregulated albumin and total protein serum levels and reduced hepatic oxidative stress with the combination being most effective. Moreover, the combination group showed enhanced wound-healing effects and almost normalized hepatic and pancreatic histopathology. Quercetin and/or liraglutide significantly decreased txnip levels and serine phosphorylation of IRS-1 and increased PI3K levels compared to the diabetic untreated group. Interestingly, only the combination therapy normalized hepatic IRS-1 expression. The combination of quercetin and liraglutide showed enhanced antidiabetic effects, possibly through lowering hepatic txnip levels, with the resultant up-regulation of the IRS-1/PI3K pathway.

关键词： diabetes IRS-1 liraglutide PI3K quercetin txnip

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Exosomal miR-17-5p from adipose-derived mesenchymal stem cells inhibits abdominal aortic aneurysm by suppressing txnip-NLRP3 inflammasome

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STEM CELL RESEARCH & THERAPY 2022年第1期13卷 349页

作者： Hu, Jiateng Jiang, Yihong Wu, Xiaoyu Wu, Zhaoyu Qin, Jinbao Zhao, Zhen Li, Bo Xu, Zhijue Lu, Xinwu Wang, Xin Liu, Xiaobing Shanghai Jiao Tong Univ Shanghai Peoples Hosp 9 Dept Vasc Surg Sch Med Shanghai Peoples R China Shanghai Jiao Tong Univ Vasc Ctr Shanghai Peoples R China

Background Preclinical studies have suggested that adipose-derived mesenchymal stem cells (ADSCs) transplantation can suppress abdominal aortic inflammation and aneurysm expansion through paracrine factors. Yet, the mechanism of action is not fully understood. In the present study, we further examined the function and mechanism of ADSC-derived exosomes (ADSC-exos) and their microRNA-17-5p (miR-17-5p) on the abdominal aortic aneurysm (AAA) progression. Methods ADSC-exos were isolated and identified. DiR and PKH67 staining were used to trace ADSC-exo in vivo and in vitro. Raw264.7 cells were applied to perform in vitro experiments, while a murine AAA model induced using angiotensin II (Ang II) was used for in vivo testing. The expression level of miR-17-5p in macrophages and Ang II-treated macrophages after ADSC-exos treatment was determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The target relation between miR-17-5p and thioredoxin-interacting protein (txnip) was identified by a dual-luciferase reporter gene assay. Artificial activation and block of experiments of miR-17-5p and txnip were conducted to clarify their functions in inflammation during AAA progression. The severity of AAA between groups was assessed by maximal aorta diameter, AAA incidence, survival rate, and histological stainings. Besides, inflammasome-related proteins and macrophage pyroptosis were further evaluated using western blot, RT-qPCR, and enzyme-linked immunosorbent assay (ELISA). Results The ADSC-exos were isolated and identified. In vivo testing showed that ADSC-exos were mainly distributed in the liver. Meanwhile, in vitro experiments suggested that ADSC-derived exosomes were taken up by macrophages, while inside, ADSC-exos miR-17-5p decreased a txnip induced by Ang II by directly binding to its 3 '-untranslated region (3'UTR). Furthermore, overexpression of miR-17-5p enhanced the therapeutic function of ADSC-exos on inflammation during AAA expansion

关键词： txnip Adipose-derived mesenchymal stem cells Exosomes microRNA-17-5p Macrophages Inflammation

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ITCH facilitates proteasomal degradation of txnip in hypoxia- induced lung cancer cells

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THORACIC CANCER 2022年第15期13卷 2235-2247页

作者： Sun, Qian Wang, Bi-Bo Wei, Wei Huang, Gui-Chun Liu, Lei-Lei Chen, Wei-Wei Wang, Jing Zhao, Xiao-Yue Lu, Lu Fang, Rong Zhu, Chun-Yan Chu, Xiao-Yuan Jinling Hosp Dept Med Oncol 305 Zhongshan East Rd Nanjing 210000 Peoples R China Jinling Hosp Dept Cardiothorac Surg Nanjing Peoples R China Nanjing Univ Jinling Hosp Med Sch Dept Med Oncol Nanjing Peoples R China Jinling Hosp Dept Pathol Nanjing Peoples R China

Background Lung cancer (LC) is one of the most common cancers and a leading cause of cancer-related deaths worldwide. In many pathological conditions, particularly in the tumor microenvironment, cells and tissues frequently exist in a hypoxic state. Here, we evaluated Itchy E3 ubiquitin protein ligase (ITCH) expression in LC cells following hypoxia treatment. Methods LC cell lines were treated with hypoxic condition. Cell migration, invasion, inflammation, reactive oxygen species (ROS) production, and apoptosis of LC cells were determined by wound healing assay, Transwell invasive assay, ELISA, DCFH-DA staining, and flow cytometry, respectively. qPCR and WB were used to determine the expression of ITCH and txnip. Co-IP was performed to assess the interaction between ITCH and txnip. Results ITCH expression was downregulated in LC cells under hypoxic conditions. Next, LC cells were subjected to hypoxic conditions and changes in cell viability and metastasis were determined. Hypoxic conditions resulted in increased migration and invasion abilities of LC cells. Intracellular reactive oxygen species (ROS) production, inflammation, and apoptosis were also promoted by hypoxia. We found that ITCH overexpression led to the proteasomal degradation of thioredoxin-interacting protein (txnip), whereas the expression of the ITCH C830A mutant did not affect txnip levels in LC cells. The gain-of-function experiment demonstrated that migration, invasion, ROS generation, inflammation, and apoptosis of hypoxia-conditioned LC cells were ameliorated by ITCH overexpression, whereas the ITCH C830A mutant did not cause any changes in these phenotypes. Furthermore, the contribution of txnip knockdown and ITCH overexpression to the hypoxia-induced features in LC cells with ITCH C830A was found to be similar. Conclusion Our results suggest a novel mechanism underlying the changes in ITCH-mediated malignant phenotypes of hypoxia-conditioned LC cells via txnip.

关键词： degradation hypoxia ITCH lung cancer txnip

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Acupuncture at ST36 Alleviates the Behavioral Disorder of Autistic Rats by Inhibiting txnip-Mediated Activation of NLRP3

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JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 2022年第2期81卷 127-134页

作者： Zhao, Pengju Fu, Hongguang Cheng, Hui Zheng, Ruijuan Yuan, Dan Yang, Jianquan Li, Sheng Li, Enyao Li, Liguo Zhengzhou Univ Dept Children Rehabil Key Lab Rehabil Med Henan Affiliated Hosp 5 3 Rehabil St Zhengzhou 450052 Peoples R China Zhengzhou Hlth Vocat Coll Inst Hlth Engn Zhengzhou Peoples R China Sichuan Univ Coll Life Sci Chengdu Peoples R China

Autism is a common neurodevelopmental disorder that severely affects patients' quality of life. We aimed to investigate whether acupuncture at Zusanli (ST36) could alleviate the behavior disorder of autistic rats by inhibiting thioredoxin-interacting protein (txnip)-mediated activation of NLRP3. An autism model was induced by intraperitoneal injection of pregnant rats with valproic acid (VPA). The pups' behaviors were analyzed using hot plate, open field, Morris water maze, and 3-chamber social interaction tests. Nissl staining was used to visualize neurons in prefrontal cortex. Levels of txnip, NLRP3, interleukin (IL)-1 beta, and caspase were determined by Western blot or quantitative real-time PCR. After ST36 acupuncture, pain sensitivity, autonomous activity, sociability index, sociability preference index, and learning and memory were improved in the autism model rats. Levels of txnip, NLRP3, IL-1 beta, and caspase 1 were decreased after acupuncture. Interference with txnip alleviated the behavior disorders and inhibited NLRP3, caspase 1, and IL-1 beta levels. In summary, ST36 acupuncture reduced txnip expression, inhibited the activation of the NLRP3 inflammasome, and alleviated the behavior disorder related to the prefrontal cortex of the autistic rats. These results point to a potential mechanism for acupuncture-induced improvement of autistic behavioral disorders.

关键词： Acupuncture Autism Behavior disorder NLRP3 txnip

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txnip promotes autophagic apoptosis in diabetic cardiomyopathy by upregulating FoxO1 and its acetylation

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CELLULAR SIGNALLING 2024年 124卷 111469页

作者： Zhang, Yaoting Li, Bing Fu, Yu Cai, He Zheng, Yang First Hosp Jilin Univ Dept Cardiovasc Dis Changchun 130021 Peoples R China

Autophagy dysfunction and apoptosis exacerbate the risk of heart failure in patients with diabetic cardiomyopathy (DCM). However, the interactions between autophagy and apoptosis in DCM and their underlying mechanisms remain poorly understood. This study induced type 1 DCM in C57BL/6 mice via streptozotocin injection and exposed H9C2 cells to high glucose to investigate these mechanisms. The study revealed a significant elevation in autophagic vesicles and compromised autophagic flux, accompanied by pronounced myocardial cell apoptosis in the myocardium of diabetic mice. Long-term exposure to high glucose in H9C2 cells led to enhanced autophagosome formation and impaired autophagic flux, while inhibition of autophagy with 3MA reduced cell apoptosis. Additionally, we observed an increase in txnip expression in the myocardium of diabetic mice and in high glucose-treated H9C2 cells, which regulates autophagic apoptosis in high glucose- treated H9C2 cells. Furthermore, txnip regulates autophagic apoptosis through the modulation of forkhead box-1 (FoxO1) expression and acetylation. Prolonged high glucose exposure resulted in increased levels of phosphorylated sirtuin 1 (SIRT1) and reduced SIRT1/FoxO1 interaction, changes that were ameliorated by txnip knockdown. txnip overexpression elevated FoxO1 levels, which could be suppressed by NAC and GSH. These findings revealed that txnip mediates autophagic apoptosis in DCM by upregulating FoxO1 via ROS and enhancing FoxO1 acetylation through the suppression of SIRT1 activity. The discovery of this new mechanism provides new perspectives and potential therapeutic targets for understanding and treating DCM.

关键词： txnip FoxO1 Acetylation Autophagy Apoptosis

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