牙龈卟啉单胞菌（P.gingivalis，Pg）为牙周病重要致病菌。人类牙龈上皮细胞(HGEC)是牙周组织防御的第一道屏障。Pg能够内化于HGEC，在细胞内生存繁殖，导致牙周感染加重。本课题组前期工作表明Pg内化HGEC后通过PI3K/AKT和JAK/STAT3信号通路，下调caspase-3/9活性，抑制细胞凋亡，细胞快速通过G1期，Cyclin D和Cyclin E提前表达和高表达，加速上皮细胞周期进程。Pg内化的HGEC抑制细胞凋亡和加速细胞周期现象是Pg感染牙周组织，达到牙周组织深层的重要机制和策略。Pg内化诱发牙龈上皮细胞p21磷酸化修饰及泛素化降解在Pg内化HGEC过程中处于中心调控点。通过研究蛋白修饰p21对HGEC细胞周期和凋亡的双重调控机制，我们期望发现一种途径阻断Pg内化HGEC细胞周期和凋亡改变，减少牙周感染加重及复发的可能。

Porphyromonas gingivalis is one of the important pathogens for perodontitis. Human gingival epithelial cell(HGEC) is the first defensive barrier of periodontal tissue.P.gingivalis is able to internalize into HGEC,then survive and proliferate in the cell,which eventually lead to a more serious periodontal infection.Our early work showed that internalization of P.gingivalis induced an inhibition of cell apoptosis with an increase in caspase-3/9 activity.The infected HGEC had quickly progressed through the G1 phase and accelerated the process of cell cycle with early and high expression of Cyclin D and Cyclin E,which was through the PI3K/AKT and JAK/STAT3 signal pathways.After P.gingivalis internalizing into HGEC,P.gingivalis inhibiting cell apoptosis and accelerating the process of cell cycle are the important mechanism and strategy of P.gingivalis infecting and invasing deep periodontal tissue.Internalization of P.gingivalis inducing phosphorylation and ubiquitin-proteasome degradation of p21 in HGEC has an important role in the process of P.gingivalis internalizing into HGEC.Studying of the protein modification of p21,we expect to find a path to inhibit cell cycle and apoptosis of HGEC internalized by P.gingivalis,in order to reduce the recurrence and exacerbation of periodontal infection.