Huang Xin, Xiao Junhong, Wang Huiyi, Peng Yan, Liu Heyu, Ma Li, Wang Xiaoxuan, Cao Zhengguo
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Department of Periodontology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
J Oral Microbiol. 2023 Jul 20;15(1):2236427. doi: 10.1080/20002297.2023.2236427. eCollection 2023.
Casein kinase 2 interacting protein-1 (CKIP-1) is a versatile player involved in various biological processes. However, whether CKIP-1 mediates the osteogenic/cementogenic differentiation of periodontal ligament cells (PDLCs) under (Pg) stimulation remains unknown.
The effect of Pg on PDLC differentiation was first verified. CKIP-1 expression in Pg-infected PDLCs or in PDL of apical periodontitis (AP) mice was detected. The changes of CKIP-1 during PDLC differentiation was also determined. PDLC differentiation capacity in knockout (KO) mice and CKIP-1-silenced PDLCs with or without Pg stimulation were further studied. Inhibitor was finally applied to verify the involvement of p38 signaling pathway in PDLC differentiation.
The suppression effect of Pg on PDLC differentiation was demonstrated. CKIP-1 increased in the PDL of AP mice and Pg-induced PDLCs, and decreased gradually during PDLC differentiation. Increased OSX and RUNX2 expression in PDL were observed in KO mice. Also, CKIP-1 silencing facilitated and rescued Pg-inhibited PDLC differentiation. Inhibitor for p38 signaling pathway blocked CKIP-1 silencing-facilitated PDLC differentiation.
CKIP-1 mediated the osteogenic/cementogenic differentiation of PDLCs partially through p38 signaling pathway, which may provide evidence for the regeneration of periodontal hard tissues damaged by Pg.
酪蛋白激酶2相互作用蛋白1(CKIP-1)是参与多种生物学过程的多功能蛋白。然而,CKIP-1是否在牙龈卟啉单胞菌(Pg)刺激下介导牙周膜细胞(PDLCs)的成骨/成牙骨质分化仍不清楚。
首先验证Pg对PDLC分化的影响。检测Pg感染的PDLCs或根尖周炎(AP)小鼠牙周膜中CKIP-1的表达。还确定了PDLC分化过程中CKIP-1的变化。进一步研究了CKIP-1基因敲除(KO)小鼠和沉默CKIP-1的PDLCs在有无Pg刺激下的PDLC分化能力。最后应用抑制剂验证p38信号通路是否参与PDLC分化。
证实了Pg对PDLC分化的抑制作用。CKIP-1在AP小鼠牙周膜和Pg诱导的PDLCs中增加,在PDLC分化过程中逐渐降低。在CKIP-1基因敲除小鼠的牙周膜中观察到OSX和RUNX2表达增加。此外,CKIP-1沉默促进并挽救了Pg抑制的PDLC分化。p38信号通路抑制剂阻断了CKIP-1沉默促进的PDLC分化。
CKIP-1部分通过p38信号通路介导PDLCs的成骨/成牙骨质分化,这可能为Pg损伤的牙周硬组织再生提供证据。