LINC01270 Regulates the NF-κB-Mediated Pro-Inflammatory Response via the miR-326/LDOC1 Axis in THP-1 Cells DOI Creative Commons
Imene Arab, Su‐Geun Lim, Kyoungho Suk

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(23), P. 2027 - 2027

Published: Dec. 8, 2024

Long intergenic noncoding (LINC)01270 is a 2278 bp transcript belonging to the subset of long (lnc)RNAs. Despite increased reports LINC01270's involvement in different diseases, evident research on its effects inflammation yet be achieved. In present study, we investigated potential role LINC01270 modulating inflammatory response human monocytic leukemia cell line THP-1. Lipopolysaccharide treatment upregulated expression, and siRNA-mediated suppression enhanced NF-κB activity subsequent production cytokines IL-6, IL-8, MCP-1. Interestingly, knockdown downregulated expression leucine zipper cancer 1 (LDOC1), novel suppressor. An analysis LINC01270/micro-RNA (miRNA)/protein interactome profile identified miR-326 as possible mediator. Synthetic RNA agents that perturb interaction among LINC01270, miR-326, LDOC1 mRNA mitigated changes caused by THP-1 cells. Additionally, luciferase reporter assay HEK293 cells further confirmed enhances activation, while overexpression has opposite effect. This study provides insight into responses lipopolysaccharide stimulation via miR-326/LDOC1 axis, which negatively regulates activation.

Language: Английский

Macrophage-derived lncRNAs in cancer: regulators of tumor progression and therapeutic targets DOI
Muath Suliman, Raed Obaid Saleh,

M Chandra

et al.

Medical Oncology, Journal Year: 2025, Volume and Issue: 42(4)

Published: March 6, 2025

Language: Английский

Citations

2
The Role of Long Non-Coding RNA in Rheumatoid Arthritis DOI Open Access
Kajetan Kiełbowski, Maciej Ćmil,

Wojciech Jerzy Biniek

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(2), P. 560 - 560

Published: Jan. 10, 2025

Rheumatoid arthritis (RA) is a chronic autoimmune disease that leads to joint damage and physical dysfunction. The pathogenesis of RA highly complex, involving genetic, epigenetic, immune, metabolic factors, among others. Over the years, research has highlighted importance non-coding RNAs (ncRNAs) in regulating gene expression. Given their dysregulation numerous conditions, ncRNAs are thought play role pathological processes. In RA, aberrant levels circulating long (lncRNAs) commonly observed peripheral blood, along with dysregulated expression blood mononuclear cells synovial tissue. This review discusses involvement lncRNAs inflammation aggressive characteristics fibroblast-like synoviocytes, key cellular population driving progression.

Language: Английский

Citations

0
Macrophage polarization regulates the pathogenesis and progression of autoimmune diseases DOI
Siwen Wu, Songyan Zhao,

Lei Hai

et al.

Autoimmunity Reviews, Journal Year: 2025, Volume and Issue: 24(7), P. 103820 - 103820

Published: April 21, 2025

Language: Английский

Citations

0
The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications DOI Creative Commons
Xiaoyan Wang, Liming Chen,

Jianming Wei

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2025, Volume and Issue: 10(1)

Published: May 22, 2025

Abstract Immune system plays a crucial role in the physiological and pathological regulation of cardiovascular system. The exploration history milestones immune diseases (CVDs) have evolved from initial discovery chronic inflammation atherosclerosis to large-scale clinical studies confirming importance anti-inflammatory therapy treating CVDs. This progress has been facilitated by advancements various technological approaches, including multi-omics analysis (single-cell sequencing, spatial transcriptome et al.) significant improvements immunotherapy techniques such as chimeric antigen receptor (CAR)-T cell therapy. Both innate adaptive immunity holds pivotal CVDs, involving Toll-like (TLR) signaling pathway, nucleotide-binding oligomerization domain-containing proteins 1 2 (NOD1/2) inflammasome RNA DNA sensing well antibody-mediated complement-dependent systems. Meanwhile, responses are simultaneously regulated multi-level regulations epigenetics (DNA, RNA, protein) other key pathways interactions among cells, between cardiac or vascular cells. Remarkably, based on basic research system, also made pre-clinical immunotherapy. review provides an overview providing in-depth insights into highlighting impact Finally, we discuss strategies targeting translational implications

Language: Английский

Citations

0
Epigenetic regulation of transcription factors involved in NLRP3 inflammasome and NF-kB signaling pathways DOI Creative Commons

John Kaszycki,

Minji Kim

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 19, 2025

The NLRP3 inflammasome and NF-κB signaling pathways play crucial roles in orchestrating inflammation immune defense.​ This review explores the intricate relationship between these epigenetic regulation, a field of growing importance understanding responses. Epigenetic modifications, including DNA methylation, histone non-coding RNAs (ncRNAs), significantly influence activity genes involved pathways, thereby modulating inflammatory provides comprehensive overview current research on how mechanisms interact with regulate pathways. It delves into advanced concepts such as RNA modifications 3D genome organization, their impact regulation. Furthermore, implications findings for developing novel therapeutic strategies targeting regulators diseases are discussed. By synthesizing recent advancements this rapidly evolving field, underscores critical role regulation highlights potential epigenetic-based therapies treating wide range conditions, autoimmune disorders cancer.

Language: Английский

Citations

0
Roles of non-coding RNAs and exosomal non-coding RNAs, particularly microRNAs, long non-coding RNAs, and circular RNAs, in pathogenic mechanisms behind chronic pain: A review DOI
Zhongkai Wang, Peng Jiao

International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: unknown, P. 141945 - 141945

Published: March 1, 2025

Language: Английский

Citations

0
Cycloastragenol Reduces Inflammation in CLP-induced Septic Mice by Suppressing TLR4 Signaling Pathways DOI
Guang‐Hong Chen, Weihong Wang, Baoyi Guan

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: 142, P. 156645 - 156645

Published: March 13, 2025

Language: Английский

Citations

0
LINC01270 Regulates the NF-κB-Mediated Pro-inflammatory Response via the miR-326/LDOC1 Axis in THP-1 Cells DOI Open Access
Imene Arab, Su‐Geun Lim, Kyoungho Suk

et al.

Published: June 24, 2024

Long intergenic noncoding (LINC)01270 is a 2278 bp transcript belonging to the subset of long (lnc)RNAs. Despite increased reports LINC01270’s involvement in different diseases, evident research on its effects inflammation yet be achieved. In present study, we investigated potential role LINC01270 modulating inflammatory response human monocytic leukemia cell line THP-1. Lipopolysaccharide treatment upregulated expression, and siRNA-mediated suppression enhanced NF-kB activity subsequent production cytokines IL-6, IL-8, MCP-1. Interestingly, knockdown downregulated expression leucine zipper cancer 1 (LDOC1), novel suppressor. An analysis LINC01270/micro-RNA (miRNA)/protein interactome profile identified miR-326 as possible mediator. Synthetic RNA agents that perturb interaction among LINC01270, miR-326, LDOC1 mRNA mitigated changes caused by THP-1 cells. Additionally, luciferase re-porter assay HEK293 cells further confirmed enhances activation, while overexpression has opposite effect. This study provides insight into responses lipopolysaccharide stimulation via miR-326/LDOC1 axis which negatively regulates activation.

Language: Английский

Citations

1
The long non-coding RNA GAS5 contributes to the suppression of inflammatory responses by inhibiting NF-κB activity DOI Creative Commons
Debora Curci, Biljana Stanković, Nikola Kotur

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: Oct. 9, 2024

Introduction Nuclear factor kappa B (NF-κB) is a key regulator of immune and inflammatory responses. Glucocorticoid drugs (GC) act through the glucocorticoid receptor (GR) as immunosuppressant also in pediatric patients inhibiting NF-κB activity. The long non-coding RNA GAS5 interacts with GR, influencing GC No data on role GR-dependent inhibition activity have been published. Methods This study investigated impact HeLa cells overexpressing GAS5, both under basal conditions during treatment. used EMSA, RNA-immunoprecipitation (RIP), Western blotting, bioinformatic analyses to assess DNA binding, GAS5-p65 interaction, signaling pathway modulation. Results overexpression increased binding untreated cells. RNA-IP confirmed direct interaction between subunit p65, suggesting potential regulatory mechanism. led downregulation target genes, TNF-α, NR3C1. treatment reduced GAS5-overexpressing cells, indicating synergistic effect. Furthermore, IκB levels p-p65/pan-p65 Discussion appears modulate complex manner, GC-induced signaling. GCs, multi-faceted, further research needed fully elucidate underlying mechanisms. These findings suggest that could be for personalized therapy, particularly conditions.

Language: Английский

Citations

1
LncRNA BRE-AS1 regulates the JAK2/STAT3-mediated inflammatory activation via the miR-30b-5p/SOC3 axis in THP-1 cells DOI Creative Commons

Jae-Joon Shin,

Kyoungho Suk, Won‐Ha Lee

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Oct. 28, 2024

Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators in numerous biological processes, including macrophage-mediated inflammatory responses, which play a critical role the progress of diverse diseases. This study focuses on regulatory function lncRNA brain and reproductive organ-expressed protein (BRE) antisense RNA 1 (BRE-AS1) modulating activation monocytes/macrophages. Employing THP-1 cell line model, we demonstrate that lipopolysaccharide (LPS) treatment significantly upregulates BRE-AS1 expression. Notably, specific knockdown via siRNA transfection enhances LPS-induced expression interleukin (IL)-6 IL-1β, while not affecting tumor necrosis factor (TNF)-α levels. selective augmentation pro-inflammatory cytokine production coincides with increased phosphorylation Janus kinase (JAK)2 signal transducer activator transcription (STAT)3. Furthermore, suppression results downregulation suppressor signaling (SOCS)3, an established inhibitor JAK2/STAT3 pathway. Bioinformatics analysis identified binding sites for miR-30b-5p both SOCS3 mRNA. Intervention synthetic fragment represents site attenuates effects knockdown. Conversely, mimic replicated attenuation outcomes. Our findings elucidate cells miR-30b-5p/SOCS3/JAK2/STAT3 pathway, proposing manipulation macrophage activity may offer novel therapeutic avenue diseases characterized by macrophage-driven pathogenesis.

Language: Английский

Citations

1