ArticleMedicine2018
1,25-dihydroxyvitamin-D3 promotes neutrophil apoptosis in periodontitis with type 2 diabetes mellitus patients via the p38/MAPK pathway.
Article in Medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- O-linked β-N-acetylglucosamine transferase regulates macrophage polarization in diabetic periodontitis:World journal of diabetes · 2025Article
- Inborn errors of immunity-related immunological mechanisms and pharmacological therapy alternatives in periodontitis.Clinical and experimental immunology · 2025Review
- Article
- Autophagy as a potential mechanism underlying the biological effect of 1,25-Dihydroxyvitamin D3 on periodontitis: a narrative review.BMC oral health · 2023Review
- Molecular systems architecture of host-microbiome interactions in periodontitis.JADA foundational science · 2023Review
- Uncovering the potential role of oxidative stress in the development of periodontitis and establishing a stable diagnostic model via combining single-cell and machine learning analysis.Frontiers in immunology · 2023Article
- Downregulation of ALDH6A1 is a New Marker of Muscle Insulin Resistance in Type 2 Diabetes Mellitus.International journal of general medicine · 2022Article
- Article
- Type I interferon regulates cytokine-delayed neutrophil apoptosis, reactive oxygen species production and chemokine expression.Clinical and experimental immunology · 2021Article
- A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity.Frontiers in immunology · 2021Review
- Immunomodulation in the Treatment of Periodontitis: Progress and Perspectives.Frontiers in immunology · 2021Review
- Modulation of miRNAs by vitamin C in H2O2‑exposed human umbilical vein endothelial cells.International journal of molecular medicine · 2020Article
- Identification of the key differentially expressed genes and pathways involved in neutrophilia.Innate immunity · 2020Article
- Vitamin D promotes the cisplatin sensitivity of oral squamous cell carcinoma by inhibiting LCN2-modulated NF-κB pathway activation through RPS3.Cell death & disease · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAbnormal neutrophils are involved in many chronic endocrine diseases, including type 2 diabetes mellitus (T2DM), and in periodontitis (PD), which is a chronic inflammatory disease in which neutrophils play a vital role. The p38 mitogen-activated protein kinase (MAPK) signaling pathway participates in the apoptosis of many inflammatory cells. Additionally, 1,25-dihydroxyvitamin-D3 (1,25VitD3) as a regulator can induce responses to infection and tumor cell apoptosis. However, the effect of 1,25VitD3 in the pathogenic relationship between T2DM and PD remains unclear. The aim of this study was to assess the effect of 1,25VitD3 on neutrophil apoptosis in patients with T2DM and PD and the p38-MAPK-relevant signaling pathway mechanism in this process in vitro.
methodsNeutrophils were stained with Wright's stain, and apoptosis was detected by flow cytometry and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining. Apoptosis- and p38-related mRNAs and proteins were examined by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blotting and ELISA. The internal relationships were analyzed using a linear regression equation and Pearson's correlation coefficient.
resultsThe highest rate of neutrophil apoptosis occurred in cultures treated with 10 mol/L 1,25VitD3 in the T2DM-PD group. The apoptosis rate in the T2DM-PD-p38 inhibitor group was higher than that in the healthy control group. Western blot, ELISA and qRT-PCR results showed that the mRNA and protein expression profiles of Caspase-3 and Bax were highly up-regulated and that Bcl-2 was down-regulated in the T2DM-PD-p38 inhibitor group. The expression levels of apoptotic mRNAs and proteins in the T2DM and T2DM-PD groups were significantly higher than those in the T2DM-p38 and T2DM-PD-p38 inhibitor groups. 1,25VitD3-induced neutrophil apoptosis and phosphorylated p38 (p-p38) expression were partially inhibited by the p38 inhibitor. Expression levels of apoptosis-related genes and p-p38 in neutrophils were positively associated with increasing concentrations of 1,25VitD3. p-p38 protein expression was positively associated with the level of serum 1,25VitD3.
conclusion1,25VitD3 could promote peripheral blood neutrophil apoptosis in patients with T2DM and PD through activation of the p38-MAPK signaling pathway in vitro.
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