Metastasis-associated lung adenocarcinoma transcript 1 induces methyl-CpG-binding domain protein 4 in mice with recurrent spontaneous abortion caused by anti-phospholipid antibody positivity DOI
Yongmei Han, Ying Wang, Chenyu Zhang

и другие.

Placenta, Год журнала: 2023, Номер 137, С. 38 - 48

Опубликована: Апрель 9, 2023

Язык: Английский

Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases DOI Creative Commons
Yuan Peng,

Mengxian Zhou,

Yang Hong

и другие.

Mediators of Inflammation, Год журнала: 2023, Номер 2023, С. 1 - 20

Опубликована: Июнь 8, 2023

Macrophages are innate immune cells in the organism and can be found almost tissues organs. They highly plastic heterogeneous participate response, thereby playing a crucial role maintaining homeostasis of body. It is well known that undifferentiated macrophages polarize into classically activated (M1 macrophages) alternatively (M2 under different microenvironmental conditions. The directions macrophage polarization regulated by series factors, including interferon, lipopolysaccharide, interleukin, noncoding RNAs. To elucidate various autoimmune diseases, we searched literature on with PubMed database. Search terms as follows: macrophages, polarization, signaling pathways, RNA, inflammation, systemic lupus erythematosus, rheumatoid arthritis, nephritis, Sjogren’s syndrome, Guillain-Barré multiple sclerosis. In present study, summarize common diseases. addition, also features recent advances particular focus immunotherapeutic potential diseases potentially effective therapeutic targets.

Язык: Английский

Процитировано

66

Epigenetic regulation and T-cell responses in endometriosis – something other than autoimmunity DOI Creative Commons
Dariusz Szukiewicz

Frontiers in Immunology, Год журнала: 2022, Номер 13

Опубликована: Июль 22, 2022

Endometriosis is defined as the presence of endometrial-like glands and stroma located outside uterine cavity. This common, estrogen dependent, inflammatory condition affects up to 15% reproductive-aged women a well-recognized cause chronic pelvic pain infertility. Despite still unknown etiology endometriosis, much evidence suggests participation epigenetic mechanisms in disease etiopathogenesis. The main rationale based on fact that heritable phenotype changes do not involve alterations DNA sequence are common triggers for hormonal, immunological, disorders, which play key role formation endometriotic foci. Epigenetic regulating T-cell responses, including methylation posttranslational histone modifications, deserve attention because tissue-resident T lymphocytes work concert with organ structural cells generate appropriate immune responses functionally shaped by organ-specific environmental conditions. Thus, failure precisely regulate cell transcription may result compromised immunological integrity an increased risk disorders. coexistence endometriosis autoimmunity well-known occurrence. Recent research results indicate regulatory (Treg) number highly active Tregs macrophages have been found peritoneal fluid from endometriosis. Elimination function imbalance between helper Th1 Th2 types reported endometria endometriosis-associated review aims present state art recognition reprogramming factor pathophysiology context T-cell-related autoimmunity. new potential therapeutic approaches modulation and/or adoptive transfer will also be outlined.

Язык: Английский

Процитировано

39

Epigenetic Alterations in Immune Cells of Systemic Lupus Erythematosus and Therapeutic Implications DOI Creative Commons

David E. Adams,

Wen-Hai Shao

Cells, Год журнала: 2022, Номер 11(3), С. 506 - 506

Опубликована: Фев. 1, 2022

Systemic lupus erythematosus (SLE) is an autoimmune disorder that characterized by autoantibody production and dysregulated immune cell activation. Although the exact etiology of SLE remains unknown, genetic, hormonal, complex environmental factors are known to be critical for pathologic In addition inherited genetic predisposition, epigenetic processes do not change genomic code, such as DNA methylation, histone modification, noncoding RNAs increasingly appreciated play important roles in pathogenesis. We herein focus on up-to-date findings lupus-associated alterations their pathophysiology development. also summarize therapeutic potential new findings. It likely advances study will help predict individual disease outcomes, promise diagnostic accuracy, design target-directed immunotherapies.

Язык: Английский

Процитировано

29

Roles of Long Non-coding RNAs in the Development of Aging-Related Neurodegenerative Diseases DOI Creative Commons
Yu‐Qing Ni, Hui Xu, You‐Shuo Liu

и другие.

Frontiers in Molecular Neuroscience, Год журнала: 2022, Номер 15

Опубликована: Март 14, 2022

Aging-related neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s (PD), Huntington’s (HD), and amyotrophic lateral sclerosis (ALS), are gradually becoming the primary burden of society cause significant health-care concerns. Aging is a critical independent risk factor for diseases. The pathological alterations diseases tightly associated with mitochondrial dysfunction, inflammation, oxidative stress, which in turn stimulates further progression Given potential research value, lncRNAs have attracted considerable attention. LncRNAs play complex dynamic roles multiple signal transduction axis neurodegeneration. Emerging evidence indicates that exert crucial regulatory effects initiation development aging-related This review compiles underlying mechanisms aging related Besides, we discuss aging. In addition, crosstalk network also explored.

Язык: Английский

Процитировано

23

MicroRNAs in Lupus Nephritis–Role in Disease Pathogenesis and Clinical Applications DOI Open Access
Benjamin Y. F. So,

Desmond Y. H. Yap,

Tak Mao Chan

и другие.

International Journal of Molecular Sciences, Год журнала: 2021, Номер 22(19), С. 10737 - 10737

Опубликована: Окт. 4, 2021

MicroRNAs (miRs) are non-coding small RNAs that act as epigenetic modulators to regulate the protein levels of target mRNAs without modifying genetic sequences. The role miRs in pathogenesis lupus nephritis (LN) is increasingly recognized and highly complex. Altered different observed blood, urine kidney tissues murine LN models patients. Accumulating evidence suggests these can modulate immune cells various key inflammatory pathways, their perturbations contribute aberrant response LN. dysregulation resident renal urinary exosomes also lead abnormal cell proliferation, inflammation fibrosis While may hold promise clinical applications patients, there still many potential limitations safety concerns for use. Further studies worthwhile examine utility diagnosis, disease activity monitoring, prognostication treatment

Язык: Английский

Процитировано

30

The immunomodulatory potential of vitamin D on Th17 lymphocytes in systemic lupus erythematosus - a literature review DOI Open Access

Octavian Ion Predescu,

Ştefan Cristian Dinescu,

Cristina Elena Bițǎ

и другие.

Medicine and Pharmacy Reports, Год журнала: 2025, Номер unknown

Опубликована: Янв. 20, 2025

This review offers insight into the complex interplay between cytokines and vitamin D, with focus on its role in systemic lupus erythematosus (SLE) pathogenesis. It a helpful resource for researchers clinicians seeking to better understand treat SLE related autoimmune conditions. The pathogenesis of is involves wide range cytokines, primarily Th2 type; these mediate hyperactivity B lymphocytes antibody production. Notably, D found suppress activity critical Th17-related like IL-23 IL-6, which pivotal Th17 cell development function. ultimately leads reduced IL-17 production, an increase regulatory T lymphocytes, subsequent secretion IL-10. Supplementation seen have positive effects SLE, leading lower disease scores, decreased levels autoantibodies, reduction fatigue.

Язык: Английский

Процитировано

0

Up-Regulated Expression of Pro-Apoptotic Long Noncoding RNA lincRNA-p21 with Enhanced Cell Apoptosis in Lupus Nephritis DOI Open Access
Yi-Cheng Chen,

Pin-Yu Kuo,

Yu‐Chi Chou

и другие.

International Journal of Molecular Sciences, Год журнала: 2020, Номер 22(1), С. 301 - 301

Опубликована: Дек. 30, 2020

Accelerated cell apoptosis with dysregulated long noncoding RNAs is the crucial pathogenesis in lupus nephritis (LN). Pro-apoptotic lincRNA-p21 was studied LN patients, lines lentivirus-mediated overexpression and CRISPR interference (CRISPRi)-conducted repression, a mouse model. Clinical samples were from patients age/sex-matched controls. Expression of endogenous RNA target miR-181a, examined mononuclear urine cells. Guide sequences targeting cloned into CRISPRi dCas9/ Krüppel-associated box (KRAB) domain. LincRNA-p21-silened transfectants investigated for miR-181a expression. LincRNA-p21-overexpressed cells evaluated p53-related down-stream molecules. Balb/C mice injected pristane to induce lincRNA-p21. Higher levels found cells, positively correlated activity. There lower negatively Doxorubicin-induced apoptotic had up-regulated levels. dCas9/KARA domain showed efficient repression ability on transcription initiation/elongation. CRISPRi-conducted lincRNA-p21-silenced displayed reduced levels, whereas lincRNA-p21-overexpressed revealed enhanced downstream PUMA/Bax glomerular progressive increased Our results demonstrate expression LN, implicating potential diagnostic marker therapeutic target.

Язык: Английский

Процитировано

31

Involvement of lncRNA IL21-AS1 in interleukin-2 and T follicular regulatory cell activation in systemic lupus erythematosus DOI Creative Commons
Hao He, Shingo Nakayamada, Naoaki Ohkubo

и другие.

Arthritis Research & Therapy, Год журнала: 2021, Номер 23(1)

Опубликована: Дек. 11, 2021

Abstract Background The single nucleotide polymorphism (SNP) rs62324212, located in IL21 antisense RNA 1 (IL21-AS1), has been identified as a genetic risk variant associated with systemic lupus erythematosus (SLE). We aimed to probe the characteristics of IL21-AS1 and explore its clinical relevance focusing on T helper subsets disease activity patients SLE. Methods rs62324212 genotyping was determined using allelic discrimination by quantitative PCR. Gene expression peripheral blood mononuclear cells cell surface markers CD4 + were analyzed PCR flow cytometry. association among IL21-AS1, subsets, SLE accessed. Results Ensembl Genome Browser analysis revealed that (C>A) predicting enhancer region IL21-AS1. expressed nucleus B cells, but decreased positively correlated mRNA levels IL-2 not IL-21, it proportion activated follicular regulatory (Tfr) cells. Furthermore, we observed significant negative correlation between ( n = 53, p < 0.05). Conclusion an effect through involvement IL-2-mediated activation Tfr Thus, targeting may provide therapeutic approaches for

Язык: Английский

Процитировано

21

Long noncoding RNA SNHG16 regulates TLR4-mediated autophagy and NETosis formation in alveolar hemorrhage associated with systemic lupus erythematosus DOI Creative Commons
Yu-Tung Hsieh, Yi‐Cheng Chen, Yu‐Chi Chou

и другие.

Journal of Biomedical Science, Год журнала: 2023, Номер 30(1)

Опубликована: Сен. 12, 2023

Dysregulated long noncoding RNA (lncRNA) expression with increased apoptosis has been demonstrated in systemic lupus erythematosus (SLE) patients alveolar hemorrhage (AH). SNHG16, a lncRNA, can enhance pulmonary inflammation by sponging microRNAs, and upregulate toll-like receptor 4 (TLR4) via stabilizing its mRNAs. TRAF6, TLR4 downstream signal transducer, induce autophagy NETosis formation. In this study, we investigated whether SNHG16 could regulate TLR4-mediated formation SLE-associated AH.Expression of TRAF6 cell death processes were examined lung tissues peripheral blood (PB) leukocytes from AH associated SLE other autoimmune diseases, the lungs spleen pristane-induced C57BL/6 mouse model. SNHG16-overexpressed or -silenced myelocytic cells stimulated lipopolysaccharide (LPS), agonist, for analyzing NETosis, respectively. Pristane-injected mice received intra-pulmonary delivery lentivirus (LV)-SNHG16 overexpression prophylactic/therapeutic infusion short hairpin (shRNA) targeting to evaluate effects on AH. Renal was also nephritis (LN) BALB/c LN model.Up-regulated SLE-AH lungs. such patients, up-regulated found PB mononuclear neutrophils NETosis. There LPS-induced cells, while down-regulated decreased SNHG16-silenced cells. had TLR4/TRAF6 levels situ Intra-pulmonary LV-SNHG16 enhanced through up-regulating processes, prophylactic early therapeutic sh-SNHG16 suppressed down-regulating reduced processes. addition, there renal mice.Our results demonstrate that lncRNA regulates human lungs, provide potential shRNA SLE-related lethal manifestation.

Язык: Английский

Процитировано

7

tRF-His-GTG-1 enhances NETs formation and interferon-α production in lupus by extracellular vesicle DOI Creative Commons
Yi‐Ming Chen, Kuo‐Tung Tang, Hung‐Jen Liu

и другие.

Cell Communication and Signaling, Год журнала: 2024, Номер 22(1)

Опубликована: Июль 7, 2024

Abstract Background Hyperactive neutrophil extracellular traps (NETs) formation plays a crucial role in active severe systemic lupus erythematosus (SLE). However, what triggers the imbalance dysregulated NETs SLE is elusive. Transfer RNA-derived small RNAs (tsRNAs) are novel non-coding RNAs, which participate various cellular processes. We explore of tsRNAs on SLE. Methods analyzed levels DNA and platelet-derived vesicles (pEVs) from 50 patients 20 healthy control subjects. The effects pEVs were evaluated by using immunofluorescence assay myeloperoxidase-DNA PicoGreen assay. regulatory mechanism inflammatory cytokines production investigated an vitro cell-based Results Increased circulating shown associated with disease activity ( P < 0.005). demonstrated that patient-derived immune complexes (ICs) induced platelet activation, followed release. ICs-triggered was significantly enhanced presence through Toll-like receptor (TLR) 8 activation. tRF-His-GTG-1 neutrophils activity. interacted TLR8 to prime p47phox phosphorylation neutrophils, resulting reactive oxygen species formation. Additionally, modulated NF-κB IRF7 activation upon engagement, IL-1β, IL-8, interferon-α upregulation, respectively. Conclusions level positively correlated patients; inhibitor could efficiently suppress formation/hyperactivation, may become potential therapeutic target.

Язык: Английский

Процитировано

2