Caspase‐3 and gasdermin E mediate macrophage pyroptosis in periodontitis

Xiangru Gao; Shuhan Li; Wenxuan Wang; Xiangyan Zhang; Xinbo Yu; Chun Fan; Wei Li; Caixiu Yang; Lei Wang; Qiuxia Ji

doi:10.1111/jre.13197

October 26, 2023Journal of Periodontal Research

Caspase‐3 and gasdermin E mediate macrophage pyroptosis in periodontitis

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Key Points

To investigate the molecular mechanisms of macrophage pyroptosis in periodontitis, focusing on the caspase-3 and gasdermin E signaling pathways.
Assessed the expression and spatial co-localization of GSDME and macrophage marker CD68 in healthy versus periodontitis gingival tissues using immunofluorescence double staining.
Treated murine RAW264.7 macrophages in vitro with Porphyromonas gingivalis lipopolysaccharide alongside NF-κB agonists or inhibitors.
Measured gene and protein levels of NF-κB, caspase-3, GSDME, and IL-1β using qRT-PCR, western blotting, and ELISA.
GSDME and CD68 were markedly elevated and co-localized within inflamed gingival tissues compared to healthy controls.
P. gingivalis-LPS stimulation significantly upregulated mRNA and protein levels of NF-κB, caspase-3, GSDME, and IL-1β in RAW264.7 macrophages.
Pretreatment with an NF-κB agonist amplified, whereas an NF-κB inhibitor suppressed, caspase-3 and GSDME expression along with downstream pyroptotic activity.

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Implication

Laboratory study demonstrates that caspase-3 and gasdermin E mediate macrophage pyroptosis in periodontitis, suggesting novel therapeutic targets for chronic gum inflammation.

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Cite This Study

Gao et al. (2023) studied this question.

synapsesocial.com/papers/6a71b77c8031ec7bb1dd161f https://doi.org/10.1111/jre.13197

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Caspase‐3 and gasdermin E mediate macrophage pyroptosis in periodontitis

Key Points

No abstract yet

Implication

Discussion

Cite This Study

Caspase‐3 and gasdermin E mediate macrophage pyroptosis in periodontitis

Key Points

No abstract yet

Implication

Discussion

Cite This Study

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