METTL3 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells Under the Inflammatory Microenvironment Through the miR-141-3p/ZEB1 Axis DOI Creative Commons
Weijia Li,

Adili Alimujiang

Cell Biochemistry and Biophysics, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 16, 2024

Periodontitis, a chronic inflammatory condition, often results in gum tissue damage and can lead to tooth loss. This study explores the role of methyltransferase-like 3 (METTL3) promoting osteogenic differentiation human periodontal ligament stem cells (hPDLSCs) within an microenvironment. An environment was simulated hPDLSCs using lipopolysaccharide (LPS). Both adipogenic capacities were assessed. In LPS-treated hPDLSCs, METTL3 overexpressed, alkaline phosphatase (ALP) staining performed alongside measurements ALP activity, pro-inflammatory cytokines, METTL3, miR-141-3p, pri-miR-141, Zinc finger E-box binding homeobox 1 (ZEB1), runt-related transcription factor 2 (RUNX2), osteocalcin (OCN). N6-methyladenosine (m6A) pri-miR-141 levels quantified, miR-141-3p ZEB1 analyzed. The demonstrated that diminished under conditions, coinciding with downregulated expression. However, overexpression enhanced differentiation. facilitated conversion into via m6A modification, resulting increased levels, which turn suppressed Inhibition or partially counteracted positive effects on conclusion, these findings suggest METTL3-mediated modification promotes microenvironment through miR-141-3p/ZEB1 axis.

Language: Английский

Epigenetic Mechanisms in Osteoporosis: Exploring the Power of m6A RNA Modification DOI Creative Commons
Shuo Tian,

Yagang Song,

Lin Guo

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2025, Volume and Issue: 29(1)

Published: Jan. 1, 2025

ABSTRACT Osteoporosis, recognised as a metabolic disorder, has emerged significant burden on global health. Although available treatments have made considerable advancements, they remain inadequately addressed. In recent years, the role of epigenetic mechanisms in skeletal disorders garnered substantial attention, particularly concerning m 6 A RNA modification. is most prevalent dynamic and reversible modification eukaryotes, mediating various processes mRNAs, including splicing, structural conversion, translation, translocation degradation serves crucial component Research increasingly validated that plays vital proliferation, differentiation, migration, invasion,and repair bone marrow mesenchymal stem cells (BMSCs), osteoblasts osteoclasts, all which impact whole process osteoporosis pathogenesis. Continuous efforts been to target regulators natural products derived from traditional medicine, exhibit multiple biological activities such anti‐inflammatory anticancer effects, valuable resources for drug discovery. This paper elaborates methylation its regulatory osteoporosis, emphasising implications diagnosis treatment, thereby providing theoretical references.

Language: Английский

Citations

0
DNA and RNA Methylation in Periodontal and Peri-implant Diseases DOI
Lena Larsson,

Paula Milena Giraldo‐Osorno,

Carlos Garaicoa‐Pazmiño

et al.

Journal of Dental Research, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 4, 2024

Periodontal and peri-implant diseases are primarily biofilm-induced pathologies in susceptible hosts affecting the periodontium dental implants. Differences disease susceptibility, severity, patterns of progression have been attributed to immune regulatory mechanisms such as epigenetics. DNA methylation is an essential epigenetic mechanism governing gene expression that plays pivotal roles genomic imprinting, chromosomal stability, apoptosis, aging. Clinical studies explored inhibitors for cancer treatment predictive profiles progression. In periodontal health, has emerged critical, evidenced by clinical unraveling its complex interplay with inflammatory genes role periodontitis contributing severity. Human shown enzymes associated reactivation (e.g., ten-eleven translocation-2) elevated compared gingivitis. Dysregulation these can lead production cytokines altered initial response bacteria via toll-like receptor signaling pathway diseases. addition, diseases, this dysregulation result levels enzymatic activity influenced properties titanium surface. Beyond traditional perspectives, recent evidence highlights involvement RNA N6-methyladenosine [m6A], N6,2′-0-dimethyladenosine [m6Am]) peri-implantitis lesions, playing vital innate response, cytokines, activation dendritic cells. Both influence expression, virulence, bacterial behavior well-known pathogens Porphyromonas gingivalis. Alterations changes metabolism, drug resistance, related survival host, thereby promoting tissue degradation chronic responses. summary, present state-of-the-art review navigates evolving landscape integrating developments reshape understanding dynamics oral health.

Language: Английский

Citations

2
CXCR4-mediated neutrophil dynamics in periodontitis DOI
Xuanwen Xu, Tiange Li,

Jingqi Tang

et al.

Cellular Signalling, Journal Year: 2024, Volume and Issue: 120, P. 111212 - 111212

Published: May 7, 2024

Language: Английский

Citations

1
N6-methyladenosine-mediated overexpression of TREM-1 is associated with periodontal disease DOI

Deepika Burra Anand,

Jaiganesh Ramamurthy, Balachander Kannan

et al.

Odontology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 26, 2024

Language: Английский

Citations

1
METTL3 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells Under the Inflammatory Microenvironment Through the miR-141-3p/ZEB1 Axis DOI Creative Commons
Weijia Li,

Adili Alimujiang

Cell Biochemistry and Biophysics, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 16, 2024

Periodontitis, a chronic inflammatory condition, often results in gum tissue damage and can lead to tooth loss. This study explores the role of methyltransferase-like 3 (METTL3) promoting osteogenic differentiation human periodontal ligament stem cells (hPDLSCs) within an microenvironment. An environment was simulated hPDLSCs using lipopolysaccharide (LPS). Both adipogenic capacities were assessed. In LPS-treated hPDLSCs, METTL3 overexpressed, alkaline phosphatase (ALP) staining performed alongside measurements ALP activity, pro-inflammatory cytokines, METTL3, miR-141-3p, pri-miR-141, Zinc finger E-box binding homeobox 1 (ZEB1), runt-related transcription factor 2 (RUNX2), osteocalcin (OCN). N6-methyladenosine (m6A) pri-miR-141 levels quantified, miR-141-3p ZEB1 analyzed. The demonstrated that diminished under conditions, coinciding with downregulated expression. However, overexpression enhanced differentiation. facilitated conversion into via m6A modification, resulting increased levels, which turn suppressed Inhibition or partially counteracted positive effects on conclusion, these findings suggest METTL3-mediated modification promotes microenvironment through miR-141-3p/ZEB1 axis.

Language: Английский

Citations

1