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Wang Q, Liu CZ, Li BT, Yu XQ, Zhang JY, Wang ZT, Liao LJ, Liu XD. Ozone controls the metabolism of tryptophan protecting against sepsis-induced intestinal damage by activating aryl hydrocarbon receptor. World J Gastroenterol 2025; 31:105411. [DOI: 10.3748/wjg.v31.i17.105411] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/21/2025] [Revised: 03/10/2025] [Accepted: 04/16/2025] [Indexed: 04/29/2025] Open
Abstract
BACKGROUND Intestinal injury is the most common complication of sepsis, and the mitigation of intestinal damage is crucial for treating sepsis.
AIM To examine the use of ozone-rich water and its action in preventing intestinal damage caused by sepsis.
METHODS Through histological analysis, immunohistochemistry, immunofluorescence assays, and Western blot detection, we evaluated the therapeutic efficacy of ozone in mitigating intestinal injury during sepsis. Additionally, by conducting 16S rRNA sequencing and untargeted metabolomics analysis on fecal samples, we identified alterations in the gut microbiota and specific metabolites in septic mice following ozone treatment. This comprehensive approach aims to further elucidate the mechanistic underpinnings of ozone therapy in alleviating sepsis-induced intestinal damage.
RESULTS Our results demonstrate that ozonated water significantly ameliorates pathological damage in intestinal tissues, enhances the expression of tight junction proteins, and inhibits the polarization of intestinal macrophages, thereby reducing the expression of inflammatory cytokines in intestinal tissues of cecal ligation and puncture-induced septic mice. 16S rRNA sequencing analysis revealed that ozonated water increased the abundance of beneficial bacteria and alleviated gut microbiota dysbiosis. Studies using broad-spectrum antibiotic-treated mice indicated that the protective effects of ozonated water on intestinal injury are dependent on the gut microbiota. Furthermore, metabolomic analysis identified an increase in the tryptophan metabolite DL-tryptophan in the ozonated water treatment group. This suggests that ozonated water protects against intestinal injury by activating the aryl hydrocarbon receptor and suppressing necroptosis in intestinal epithelial cells.
CONCLUSION Ozone protected against sepsis-induced intestinal injury through regulation of the gut microbiota and tryptophan metabolism, inhibiting necrotic apoptosis of intestinal epithelial cells through activation of the aryl hydrocarbon receptor.
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Affiliation(s)
- Qing Wang
- Department of Anesthesiology and Pain Management, Shanghai East Hospital, Shanghai 200433, China
| | - Chun-Zheng Liu
- Department of Anesthesiology and Pain Management, Shanghai East Hospital, Shanghai 200433, China
| | - Bai-Tian Li
- Department of Anesthesiology and Pain Management, Shanghai East Hospital, Shanghai 200433, China
| | - Xiu-Qin Yu
- Department of Anesthesiology and Pain Management, Shanghai East Hospital, Shanghai 200433, China
| | - Jin-Yuan Zhang
- Department of Anesthesiology and Pain Management, Shanghai East Hospital, Shanghai 200433, China
| | - Ze-Tian Wang
- Department of Anesthesiology and Pain Management, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200240, China
| | - Li-Jun Liao
- Department of Pain Management, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200433, China
| | - Xiao-Dong Liu
- Department of Anesthesia and Intensive Care, The Chinese University of Hong Kong; Peter Hung Pain Research Institute
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2
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Vijayaraghavan M, Gadad SS, Dhandayuthapani S. Long non-coding RNA transcripts in Mycobacterium tuberculosis-host interactions. Noncoding RNA Res 2025; 11:281-293. [PMID: 39926616 PMCID: PMC11803167 DOI: 10.1016/j.ncrna.2024.12.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/25/2024] [Revised: 10/24/2024] [Accepted: 12/08/2024] [Indexed: 02/11/2025] Open
Abstract
Tuberculosis (TB) persists as a significant health threat, affecting millions of people all over the world. Despite years of control measures, the elimination of TB has become a difficult task as morbidity and mortality rates remain unaffected for several years. Developing new diagnostics and therapeutics is paramount to keeping TB under control. However, it largely depends upon understanding the pathogenic mechanisms of Mycobacterium tuberculosis (Mtb), the causative agent of TB. Mtb is an intracellular pathogen capable of subverting the defensive functions of the immune cells, and it can survive and multiply within humans' mononuclear phagocytes. Emerging evidence indicates that long non-coding RNAs (lncRNAs), a class of RNA molecules with limited coding potential, are critical players in this intricate game as they regulate gene expression at transcriptional and post-transcriptional levels and also by chromatin modification. Moreover, they have been shown to regulate cellular processes by controlling the function of other molecules, such as DNA, RNA, and protein, through binding with them. Recent studies have shown that lncRNAs are differentially regulated in the tissues of TB patients and cells infected in vitro with Mtb. Some dysregulated lncRNAs are associated with essential roles in modulating immune response, apoptosis, and autophagy in the host cells, adding a new dimension to TB pathogenesis. In this article, we provide a comprehensive review of the recent literature in this field and the impact of lncRNAs in unraveling pathogenic mechanisms in TB. We also discuss how the studies involving lncRNAs provide insight into TB pathogenesis, especially Mtb-host interactions.
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Affiliation(s)
- Mahalakshmi Vijayaraghavan
- Center of Emphasis in Cancer, Department of Molecular and Translational Medicine, Texas Tech University Health Sciences Center El Paso, Texas-79905, USA
| | - Shrikanth S. Gadad
- Center of Emphasis in Cancer, Department of Molecular and Translational Medicine, Texas Tech University Health Sciences Center El Paso, Texas-79905, USA
- Frederick L. Francis Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center El Paso, Texas-79905, USA
- Mays Cancer Center, UT Health San Antonio MD Anderson Cancer Center, San Antonio, TX 78229, USA
| | - Subramanian Dhandayuthapani
- Center of Emphasis in Infectious Diseases, Department of Molecular and Translational Medicine, Texas Tech University Health Sciences Center El Paso, Texas-79905, USA
- Frederick L. Francis Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center El Paso, Texas-79905, USA
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He T, Pu J, Ge H, Liu T, Lv X, Zhang Y, Cao J, Yu H, Lu Z, Du F. Elevated circulating LncRNA NORAD fosters endothelial cell growth and averts ferroptosis by modulating the miR-106a/CCND1 axis in CAD patients. Sci Rep 2024; 14:24223. [PMID: 39414920 PMCID: PMC11484692 DOI: 10.1038/s41598-024-76243-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2024] [Accepted: 10/11/2024] [Indexed: 10/18/2024] Open
Abstract
Atherosclerosis is a leading cause of cardiovascular diseases, characterized by endothelial dysfunction and lipid accumulation. Long non-coding RNAs (lncRNAs) are emerging as key regulators of endothelial cell behavior. This study aimed to investigate the role of lncRNA NORAD in endothelial cell proliferation and as a potential therapeutic target for atherosclerosis. A total of 75 CAD patients and 76 controls were recruited, and plasma NORAD levels were measured using qRT-PCR. HUVECs were transfected with si-NORAD to evaluate its effects on cell cycle, proliferation, migration, and apoptosis. Plasma NORAD levels were significantly elevated in CAD patients. The NORAD-miRNA-mRNA ceRNA regulatory network was constructed based on GEO database, and G1/S-specific cyclin-D1 (CCND1) was identified as one of the hub factors. NORAD deficiency suppressed cell migration and induced G1 cell cycle arrest in HUVECs by downregulating CCND1 in vitro. NORAD upregulated CCND1 in HUVECs via sponging miR-106a that inhibited cell migration. The dual-luciferase assay confirmed the direct targeting of miR-106a by NORAD, and overexpression of miR-106a inhibited HUVEC proliferation and migration. Si-NORAD transfection resulted in induced early apoptosis, increased intracellular ROS levels, decreased GSH levels, and reduced mitochondrial membrane potential. Additionally, si-NORAD decreased the expression of GPX4, FTH1, KEAP1, NCOA4, and Nrf2, while increasing Xct levels, confirming the involvement of ferroptosis. Our findings reveal that NORAD plays a critical role in endothelial cell proliferation, migration, and apoptosis, and its silencing induces ferroptosis. The regulatory network involving NORAD, miR-106a, and their target genes provides a potential therapeutic avenue for atherosclerosis.
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Affiliation(s)
- Tao He
- Department of Cardiology of Zhongnan Hospital, Institute of Myocardial Injury and Repair, Wuhan University, Wuhan, 430071, China
| | - Junxing Pu
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China
| | - Haijing Ge
- Department of Cardiology of Zhongnan Hospital, Institute of Myocardial Injury and Repair, Wuhan University, Wuhan, 430071, China
| | - Tianli Liu
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China
| | - Xintong Lv
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China
| | - Yu Zhang
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China
| | - Jia Cao
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China
| | - Hong Yu
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China
| | - Zhibing Lu
- Department of Cardiology of Zhongnan Hospital, Institute of Myocardial Injury and Repair, Wuhan University, Wuhan, 430071, China.
| | - Fen Du
- Department of Biochemistry and Molecular Biology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, Hubei, China.
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Zhao X, Lin W, Zhou W. Clinical significance of long non-coding RNA NORAD in rheumatoid arthritis. Adv Rheumatol 2024; 64:9. [PMID: 38238863 DOI: 10.1186/s42358-024-00349-z] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2023] [Accepted: 01/08/2024] [Indexed: 01/23/2024] Open
Abstract
BACKGROUND Rheumatoid arthritis (RA) is a chronic autoimmune disease that may cause joint deformities and seriously affect the normal life of the patients. In order to enable patients to receive timely attention and treatment, this study developed new diagnostic markers by exploring the expression and molecular mechanism of the long non-coding RNA NORAD (NORAD) in RA. METHODS Participants including 77 RA patients and 52 healthy persons were enrolled, and the corresponding clinical data and serum samples were obtained. The NORAD and miR-204-5p expression were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). The content of inflammatory cytokines (IL-6, TNF-α) were determined through enzyme-linked immunosorbent assay (ELISA). Luciferase activity reporter assay demonstrated the association between NORAD and miR-204-5p. In addition, receiver operating characteristic (ROC) curve was used to evaluate the diagnostic efficacy of NORAD, and Pearson's correlation analysis was applied for the correlation analysis. RESULTS NORAD was enriched in RA serum with high diagnostic value. Simultaneously, IL-6 and TNF-α levels were also upregulated (P < 0.001). The C-reactive protein (CRP), rheumatoid factor (RF), erythrocyte sedimentation rate (ESR) and anti-cyclic citrullinated peptide antibody (Anti-CCP) levels in RA patients were generally elevated (P < 0.001). NORAD was positively correlated with the levels of clinical indicators and inflammatory factors (P < 0.0001). Mechanistically, NORAD may affect the progression of RA by targeting and negatively regulating miR-204-5p. CONCLUSIONS There is a correlation between NORAD and the processes of RA, and NORAD has the potential to predict and diagnose the occurrence of RA.
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Affiliation(s)
- Xueru Zhao
- Department of Joint Surgery, Lishui People's Hospital, No.1188, Liyang Road, 323000, Lishui, Zhejiang, China.
| | - Weiyi Lin
- Department of Emergency Medicine, Lishui Municipal Central Hospital, 323000, Lishui, Zhejiang, China
| | - Wenhui Zhou
- Department of Joint Surgery, Lishui People's Hospital, No.1188, Liyang Road, 323000, Lishui, Zhejiang, China
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5
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Zhang T, Huang H, Liang L, Lu H, Liang D. Long non-coding RNA (LncRNA) non-coding RNA activated by DNA damage (NORAD) knockdown alleviates airway remodeling in asthma via regulating miR-410-3p/RCC2 and inhibiting Wnt/β-catenin pathway. Heliyon 2024; 10:e23860. [PMID: 38261955 PMCID: PMC10796956 DOI: 10.1016/j.heliyon.2023.e23860] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2023] [Revised: 12/14/2023] [Accepted: 12/14/2023] [Indexed: 01/25/2024] Open
Abstract
Background Asthma is a chronic inflammatory disorder with high prevalence in childhood. Airway remodeling, an important structural change of the airways, is resulted from epithelial-mesenchymal transition. Long non-coding RNA non-coding RNA activated by DNA damage (NORAD) has been found to promote epithelial-mesenchymal transition in multiple cancers. This study aimed to analyze the role of NORAD in asthma, mainly focusing on epithelial-mesenchymal transition-mediated airway remodeling, and further explored the NORAD-miRNA-mRNA network. Methods NORAD expression was analyzed in transforming growth factor-β1-induced BEAS-2B human bronchial epithelial cells and ovalbumin-challenged asthmatic mice. The influences of NORAD on the epithelial-mesenchymal transition characteristics and Wnt/β-catenin pathway activation were analyzed in vitro. The interactions between NORAD and miR-410-3p as well as miR-410-3p and regulator of chromosome condensation 2 were detected by dual-luciferase reporter assay and RNA pull-down assay. Rescue experiments using miR-410-3p antagonist and chromosome condensation 2 overexpression were used to confirm the mechanism of NORAD. Additionally, the role and mechanism of NORAD were further evaluated in asthmatic mice. Results NORAD expression was elevated in both asthmatic models. Knockdown of NORAD impeded spindle-like morphology changes, elevated E-cadherin expression, decreased N-cadherin expression, suppressed cell migration, and inactivated the Wnt/β-catenin pathway in transforming growth factor-β1-stimulated BEAS-2B cells. NORAD acted as a sponge of miR-410-3p to regulate chromosome condensation 2 expression. Rescue assays demonstrated that silencing of NORAD ameliorated transforming growth factor-β1-induced EMT via miR-410-3p/chromosome condensation 2/Wnt/β-catenin axis. In vivo, knockdown of NORAD led to the reduction of inflammatory cell infiltration and collagen deposition, suppression of IL-4, IL-13, transforming growth factor-β1 and immunoglobulin E production, decreasing of N-cadherin, chromosome condensation 2, β-catenin and c-Myc expression, but increasing of E-cadherin and miR-410-3p expression. Conclusions Silencing of NORAD alleviated epithelial-mesenchymal transition-mediated airway remodeling in asthma via mediating miR-410-3p/chromosome condensation 2/Wnt/β-catenin pathway.
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Affiliation(s)
- Ting Zhang
- Department of Respiratory, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou 450000, China
| | - Han Huang
- Department of Respiratory, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou 450000, China
| | - Lihong Liang
- Department of Respiratory, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou 450000, China
| | - Hongxia Lu
- Department of Respiratory, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou 450000, China
| | - Dongge Liang
- Department of Respiratory, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou 450000, China
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Antonakos N, Gilbert C, Théroude C, Schrijver IT, Roger T. Modes of action and diagnostic value of miRNAs in sepsis. Front Immunol 2022; 13:951798. [PMID: 35990654 PMCID: PMC9389448 DOI: 10.3389/fimmu.2022.951798] [Citation(s) in RCA: 15] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2022] [Accepted: 07/08/2022] [Indexed: 11/13/2022] Open
Abstract
Sepsis is a clinical syndrome defined as a dysregulated host response to infection resulting in life-threatening organ dysfunction. Sepsis is a major public health concern associated with one in five deaths worldwide. Sepsis is characterized by unbalanced inflammation and profound and sustained immunosuppression, increasing patient susceptibility to secondary infections and mortality. microRNAs (miRNAs) play a central role in the control of many biological processes, and deregulation of their expression has been linked to the development of oncological, cardiovascular, neurodegenerative and metabolic diseases. In this review, we discuss the role of miRNAs in sepsis pathophysiology. Overall, miRNAs are seen as promising biomarkers, and it has been proposed to develop miRNA-based therapies for sepsis. Yet, the picture is not so straightforward because of the versatile and dynamic features of miRNAs. Clearly, more research is needed to clarify the expression and role of miRNAs in sepsis, and to promote the use of miRNAs for sepsis management.
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Affiliation(s)
| | | | | | | | - Thierry Roger
- Infectious Diseases Service, Department of Medicine, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
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Zhou C, Wu D. Abnormal expression of lncRNA CASC9 in pneumonia children with respiratory failure and its feasible value for the clinical diagnosis of patients. Cell Cycle 2022; 21:1879-1886. [PMID: 35587261 DOI: 10.1080/15384101.2022.2078616] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/03/2022] Open
Abstract
lncRNA CASC9 expression was involved in a variety of diseases and exerted a protective role against inflammation and sepsis-induced injury. However, the role of CASC9 in severe pneumonia remains unclear. This study aimed to explore the potential diagnostic role of lncRNA CASC9 in severe pneumonia. The CASC9 expression levels were measured by RT-qPCR. The receiver operating characteristic curve (ROC) was conducted to evaluate the clinical diagnostic value of CASC9 in severe pneumonia. LPS-induced human lung fibroblast MRC-5 was used to establish the pneumonia model and then transfected with CASC9 overexpression vectors to evaluate the influence of CASC9 on cell viability and apoptosis. The inflammatory cytokines IL-1β, TNF-α, IL-6 levels were detected using a commercial enzyme-linked immunosorbent assay (ELISA). Pearson correlation analysis was used to explore the correlation between CASC9 expression and clinical data. The relative expression of CASC9 was downregulated in serum samples of severe pneumonia patients. The low expression of CASC9 in severe pneumonia was negatively correlated with several clinical data. The CASC9 had the relatively high area under ROC curve (AUC) values for distinguishing severe pneumonia from pneumonia children and healthy control. The elevated expression of CASC9 accelerated cell viability and diminished apoptosis in LPS-induced MRC-5 cells. The CASC9 expression was decreased in serum samples of severe pneumonia, and upregulation of CASC9 facilitated LPS-induced cell viability and inhibited apoptosis. In summary, CASC9 might be a diagnostic predictor and might act as a crucial regulatory roles in the progression of severe pneumonia.
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Affiliation(s)
- Chi Zhou
- Department of Pediatrics, Zhuji Maternity and Child Care Hospital, Zhejiang, China
| | - Danfei Wu
- Department of Pediatrics, Zhuji Maternity and Child Care Hospital, Zhejiang, China
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Sun W, He X, Zhang X, Wang X, Lin W, Wang X, Liang Y. Diagnostic value of Long non-coding Ribonucleic Acid non-coding activated by Deoxyribonucleic Acid damage in pulmonary tuberculosis and its regulatory role in Mycobacterium tuberculosis infection of macrophages. Microbiol Immunol 2022; 66:433-441. [PMID: 35568971 DOI: 10.1111/1348-0421.12986] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/10/2022] [Revised: 05/11/2022] [Accepted: 05/11/2022] [Indexed: 11/29/2022]
Abstract
Pulmonary tuberculosis (PTB) infection is a chronic inflammatory response caused by Mycobacterium tuberculosis (Mtb). The purpose of this study was to confirm the value of Long non-coding RNA (LncRNA) non-coding activated by DNA damage (NORAD) in the diagnosis of PTB and to explore its mechanism in Mtb-infected macrophages. NORAD serum levels were estimated by qRT-PCR in 90 PTB patients and 85 healthy individuals. ROC curves were employed to assess the diagnostic value of NORAD for PTB. Human and murine macrophages were infected with Mtb strain H37Rv. CCK-8 and ELISA detected macrophages viability and inflammatory cytokine secretion. A dual-luciferase reporter assay was performed to analyze the targeting relationship between NORAD and microRNA (miR)-618. NORAD was significantly elevated in patients with PTB, and its positivity was correlated with inflammatory cytokines IL-1 β (r = 0.854), TNF-α (r = 0.617), IL-6 (r = 0.585). With an AUC of 0.918, and sensitivity and specificity of 80.0% and 89.4%, respectively, NORAD remarkedly identified PTB patients from healthy individuals. Furthermore, Mtb infection significantly increased NORAD levels in THP-1 and RAW264.7 and increased their viability and inflammation (P <0.001). However, this increased effect was weakened by reduced NORAD. Dual-luciferase reporter assay confirmed that miR-618 in macrophages was a target miRNA for NORAD and can be negatively regulated by it. Moreover, elevated miR-618 suppressed macrophage viability and inflammation in Mtb infection. NORAD is a potential diagnostic biomarker for PTB and is involved in Mtb infected macrophage activity and inflammation by targeting miR-618. This article is protected by copyright. All rights reserved.
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Affiliation(s)
- Wenna Sun
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
| | - Xiong He
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
| | - Xiushuang Zhang
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
| | - Xiaomeng Wang
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
| | - Wen Lin
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
| | - Xiaofeng Wang
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
| | - Yan Liang
- Senior Department of Tuberculosis, The 8th Medical Center of PLA General Hospital, Beijing, China
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Xie Z, Wei L, Chen J, Chen Z. LncRNA NORAD deficiency alleviates kidney injury in mice and decreases the inflammatory response and apoptosis of lipopolysaccharide-stimulated HK-2 cells via the miR-577/GOLPH3 axis. Cytokine 2022; 153:155844. [DOI: 10.1016/j.cyto.2022.155844] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/27/2021] [Revised: 02/21/2022] [Accepted: 02/23/2022] [Indexed: 12/13/2022]
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Xu J, Liu XY, Zhang Q, Liu H, Zhang P, Tian ZB, Zhang CP, Li XY. Crosstalk Among YAP, LncRNA, and Tumor-Associated Macrophages in Tumorigenesis Development. Front Oncol 2022; 11:810893. [PMID: 35071016 PMCID: PMC8770286 DOI: 10.3389/fonc.2021.810893] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2021] [Accepted: 12/13/2021] [Indexed: 12/14/2022] Open
Abstract
Long non-coding RNAs (ncRNAs), which do not encode proteins, regulate cell proliferation, tumor angiogenesis, and metastasis and are closely associated with the development, progression, and metastasis of many cancers. Tumor-associated macrophages (TAMs) in the tumor microenvironment play an important role in cancer progression. The Hippo signaling pathway regulates cell proliferation and apoptosis, maintains tissue and organ size, and homeostasis of the internal environment of organisms. Abnormal expression of Yes-associated protein (YAP), the Hippo signaling pathway key component, is widely observed in various malignancies. Further, TAM, lncRNA, and YAP are currently valuable targets for cancer immunotherapy. In this review, we have logically summarized recent studies, clarified the close association between the three factors and tumorigenesis, and analyzed the outlook of tumor immunotherapy.
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Affiliation(s)
- Jing Xu
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China.,Innovation Platform of Marine Drug Screening & Evaluation, Qingdao Pilot National Laboratory for Marine Science and Technology, Qingdao, China
| | - Xin-Yuan Liu
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
| | - Qi Zhang
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
| | - Hua Liu
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
| | - Peng Zhang
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
| | - Zi-Bin Tian
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
| | - Cui-Ping Zhang
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
| | - Xiao-Yu Li
- Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China
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Ghafouri-Fard S, Khoshbakht T, Hussen BM, Taheri M, Arefian N. Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis. Front Immunol 2021; 12:798713. [PMID: 34956235 PMCID: PMC8695688 DOI: 10.3389/fimmu.2021.798713] [Citation(s) in RCA: 31] [Impact Index Per Article: 7.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2021] [Accepted: 11/19/2021] [Indexed: 12/22/2022] Open
Abstract
Sepsis is resulted from a systemic inflammatory response to bacterial, viral, or fungal agents. The induced inflammatory response by these microorganisms can lead to multiple organ system failure with devastating consequences. Recent studies have shown altered expressions of several non-coding RNAs such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs) during sepsis. These transcripts have also been found to participate in the pathogenesis of multiple organ system failure through different mechanisms. NEAT1, MALAT1, THRIL, XIST, MIAT and TUG1 are among lncRNAs that participate in the pathoetiology of sepsis-related complications. miR-21, miR-155, miR-15a-5p, miR-494-3p, miR-218, miR-122, miR-208a-5p, miR-328 and miR-218 are examples of miRNAs participating in these complications. Finally, tens of circRNAs such as circC3P1, hsa_circRNA_104484, hsa_circRNA_104670 and circVMA21 and circ-PRKCI have been found to affect pathogenesis of sepsis. In the current review, we describe the role of these three classes of noncoding RNAs in the pathoetiology of sepsis-related complications.
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Affiliation(s)
- Soudeh Ghafouri-Fard
- Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Tayyebeh Khoshbakht
- Phytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Bashdar Mahmud Hussen
- Department of Pharmacognosy, College of Pharmacy, Hawler Medical University, Erbil, Iraq.,Center of Research and Strategic Studies, Lebanese French University, Erbil, Iraq
| | - Mohammad Taheri
- Institute of Human Genetics, Jena University Hospital, Jena, Germany
| | - Normohammad Arefian
- Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
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