ArticleHuman genomics2021
Cathelicidin antimicrobial peptide (CAMP) gene promoter methylation induces chondrocyte apoptosis.
Article in Human genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Apoptosis Modulation by LL-37: From Mitochondrial Cell Death to Prosurvival Signaling.International journal of molecular sciences · 2026Review
- Overcoming LPS-mediated resistance in gram-negative pathogens: a review of LL-37 analogs and computational design strategies.Archives of microbiology · 2026Review
- Single-cell RNA sequencing of healthy and diseased rat temporomandibular joint condyle cartilage.PloS one · 2026Article
- Integrated bioinformatics and network pharmacology to identify and validate macrophage polarization related hub genes in the treatment of osteoarthritis with Astragalus membranaceus.Journal of orthopaedic surgery and research · 2025Article
- Progress in multi-omics studies of osteoarthritis.Biomarker research · 2025Review
- The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies.Journal of inflammation research · 2025Review
- Review
- mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model.International journal of experimental pathology · 2023Article
- Centenarian clocks: epigenetic clocks for validating claims of exceptional longevity.GeroScience · 2023Article
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Biological analysis of the potential pathogenic mechanisms of Infectious COVID-19 and Guillain-Barré syndrome.Frontiers in immunology · 2023Article
- Tanshinone IIA alleviates chondrocyte apoptosis and extracellular matrix degeneration by inhibiting ferroptosis.Open life sciences · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe occurrence of osteoarthritis is related to genetic and environmental factors. Among them, the change of chondrocyte gene expression pattern regulated by epigenetic modification is an important participant. This study analyzed the effect of CAMP gene methylation on the level of oxidative stress and inflammation of chondrocytes.
methodsWe analyzed the changes of the transcriptome in the articular cartilage tissue of osteoarthritis (OA) patients from the GSE117999 dataset. The GSE48422 dataset was used to analyze the changes in the methylation level of osteoarthritis cells. Cell Counting Kit-8 (CCK-8) and flow cytometry analysis of short hairpin RNA (shRNA) silencing CAMP gene and 5-μM 5-Aza-2'-Deoxycytidine (AZA) treatment on the proliferation and apoptosis of Human chondrocytes osteoarthritis (HC-OA) cells. The Dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay was used to detect the level of reactive oxygen species (ROS), and the expression level of inflammatory factors was analyzed by Western Blot.
resultsThe expression of CAMP in cartilage tissue of OA patients was upregulated, and the level of methylation was downregulated. CAMP was highly expressed in osteoarthritis articular cartilage cells. Silencing CAMP inhibited the proliferation of HC-OA cells and promoted their apoptosis. CAMP gene methylation inhibited ROS levels and tumor necrosis factor-α (TNF-α) expression levels in HC-OA cells, and promoted transforming growth factor beta (TGF-β) expression. CAMP gene methylation inhibited the proliferation of HC-OA cells and promoted their apoptosis.
conclusionCAMP gene promoter methylation inhibits ROS levels and inflammation and induces chondrocyte apoptosis.
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