Altered expression of STAT genes in periodontitis

Gholami, Leila; Movafagh, Abolfazl; Badrlou, Elham; Nazer, Naghme; Yari, Mohsen; Sadeghi, Ghasem; Mirzajani, Sara; Shadnoush, Mahdi; Sayad, Arezou; Ghafouri‐Fard, Soudeh

doi:10.3233/hab-210444

Cited by 2 publications

(1 citation statement)

References 22 publications

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“…STAT is a group of proteins involved in cellular signal transduction and regulation of immune responses [39]. In the oral cavity, the regulation of the immune system is crucial for maintaining oral health, and immune regulation processes related to STAT may have an impact on the development of periodontitis [40]. Although there is no explicit research extensively elucidating the direct relationship between STAT and periodontitis, it is a reasonable assumption that STAT may may be involved in pathogenesis of periodontitis [41].…”

Section: Discussionmentioning

confidence: 99%

LAX1 as a Core Biomarker in Alzheimer's Disease and Periodontitis via the STAT signaling pathway

Guo,

Wang

et al. 2024

Preprint

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Background: Periodontitis, an inflammatory condition affecting gums and tooth-supporting tissues, is linked to systemic health problems like cardiovascular diseases and Alzheimer's disease, a neurodegenerative disorder causing cognitive decline. The etiology of both conditions remains unclear. Methods: Download Alzheimer's datasets GSE138260 and GSE203206, and periodontitis datasets GSE53849 and GSE173078 from GEO. Utilize Weighted Gene Co-expression Network Analysis to obtain Important modules. Conduct Gene Set Enrichment Analysis to explore biological processes and pathways associated with differentially expressed genes. Apply integrated bioinformatics methods to perform CIBERSORT analysis on merged periodontitis datasets and linear support vector regression for immune cell subtype deconvolution. Validate LAX1's role in periodontitis and Alzheimer's disease through cell experiments using LAX1 overexpression plasmids and silencing siRNA. Assess expression changes in LAX1-related signaling pathways, inflammatory molecules, and apoptosis proteins via western blotting (WB). Results: GSEA results indicate enrichment of differentially expressed genes in apoptosis, neuroregulation, inflammation, neuroactive ligand-receptor interaction, and Jak-STAT signaling pathways. Venn diagram identifies core gene LAX1. Heatmap shows high expression of LAX1 in Alzheimer's and periodontitis samples. WB reveals LAX1 positively correlates with STAT pathway, activating it. Compared to Control group (CON), Glial cells from Alzheimer's disease mice (AD group) and periodontitis groups exhibit elevated IL-1, TNF-α, and IL-6, exacerbating inflammation with increased LAX1 expression. Conversely, inflammation decreases. This suggests LAX1 promotes inflammation. Compared to CON, AD and groups show downregulation of P53, Caspase-3, and FAS. Upregulation of LAX1 leads to increased expression of P53, Caspase-3, and FAS, promoting apoptosis. Conversely, apoptosis slows down. These results indicate LAX1 promotes apoptosis. Conclusion: LAX1 may serve as a core biomarker in Alzheimer's disease and periodontitis. LAX1 activates the STAT signaling pathway, promoting inflammatory responses and apoptosis.

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Section: Discussionmentioning

confidence: 99%

LAX1 as a Core Biomarker in Alzheimer's Disease and Periodontitis via the STAT signaling pathway

Guo,

Wang

et al. 2024

Preprint

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Dynamic changes in macrophage polarization during the resolution phase of periodontal disease

Uttamani,

Kulkarni,

Valverde

et al. 2024

Immunity Inflam & Disease

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AimPolarization of macrophages (Mφ) is a well‐controlled axis with considerable consequences in both the pro‐inflammatory and resolution phases of inflammation. We aimed to determine if periodontal therapy may instigate M1 to M2 Mφ polarization favoring resolution of inflammation within periodontal tissues.MethodsGingival biopsies were excised from subjects diagnosed with Stage III, Grade B periodontitis before and 4–6 weeks after nonsurgical periodontal therapy. Total RNA was isolated and pro‐ and anti‐inflammatory markers associated with Mφ polarization assessed by RT‐qPCR. Mice were subject to ligature‐induced periodontitis and gingival tissues collected after 8 days in‐situ or 10 days after ligature removal and M1 and M2 Mφ markers examined by RT‐qPCR and flow cytometry.ResultsIn human samples, improvement in clinical parameters posttherapy correlates with reduced bacterial burden, downregulation in M1 (TNF‐α, STAT1, CXCL10, and miR‐155), and elevated levels of M2 (STAT6, TGM2, CCL22, and IL‐10) Mφ markers. In a murine model of resolution of LIP, we observed reduced levels of M1 Mφ markers cox2, iNOS2, F4/80+CD80+, and F4/80+CD86+ and elevated levels of M2‐like Mφ markers tgm2, arg1, F4/80+CD206+ and F4/80+CD163+ corroborated human findings.ConclusionResolution of periodontal inflammation is associated with M1 to M2 Mφ polarization after nonsurgical periodontal therapy. Assessment of Mφ markers can provide relevant clinical information on the successful response of periodontal therapy and may be used to target nonresponders.

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Altered expression of STAT genes in periodontitis

Cited by 2 publications

References 22 publications

LAX1 as a Core Biomarker in Alzheimer's Disease and Periodontitis via the STAT signaling pathway

LAX1 as a Core Biomarker in Alzheimer's Disease and Periodontitis via the STAT signaling pathway

Dynamic changes in macrophage polarization during the resolution phase of periodontal disease

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