Regulation of Folliculin Interacting Protein 1 on Periodontitis

doi:10.13701/j.cnki.kqyxyj.2025.06.012

Abstract

Abstract: Objective: To explore the role and mechanism of folliculin interacting protein 1 (FNIP1) in periodontitis. Methods: Gingival tissues were collected from healthy volunteers and periodontitis patients. FNIP1 expression in the gingival tissues was detected by immunohistochemistry. Human periodontal stem cells (PDLSCs) were divided into control group (Con), Porphyromonas gingivalis group (P.g), FNIP1 siRNA group, P.g+FNIP1 siRNA group, and P.g+FNIP1 siRNA+Compound C (AMPK inhibitor) group. Western blot was used to detect the expression of FNIP1, tumor necrosis factor-α (TNF-α), adenosine 5‘-monophosphate-activated protein kinase (AMPK), p-AMPK, peroxisome proliferators-activated receptor γ coactivator 1 lalpha (PGC-1α), and factors associated with mitochondrial. Flow cytometry and confocal microscopy were used to detect the reactive oxygen species (ROS) content and mitochondrial membrane potential changes. Results: Compared with healthy gingiva, FNIP1 expression was significantly increased in periodontitis’s gingival tissues. P.g could increase the expression of FNIP1 and TNF-α in PDLSCs, decrease the expression of p-AMPK and PGC-1α, leading to mitochondrial dysfunction. FNIP1 siRNA could alleviate these phenomenons (P<0.05). However, Compound C could counteract the alleviation of FNIP1 siRNA partially. Conclusion: FNIP1 can regulate the inflammation and mitochondrial dysfunction of periodontal ligament stem cells through the AMPK pathway. Inhibiting FNIP1 may be able to alleviate the development of periodontitis.

Key words: folliculin interacting protein 1, adenosine 5‘-monophosphate-activated protein kinase, periodontitis, Porphyromonas gingivalis, periodontal ligament stem cells

ZHANG Caixia, ZHOU Yiwen, WEN Juan, HUANG Ziwei, LIN Shuang, YANG Ren, LI Huang, LI Guifeng. Regulation of Folliculin Interacting Protein 1 on Periodontitis[J]. Journal of Oral Science Research, 2025, 41(6): 521-528.

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