Abnormal mitochondrial structure and function are retained in gingival tissues and human gingival fibroblasts from patients with chronic periodontitis
Abnormal mitochondrial structure and function are retained in gingival tissues and human gingival fibroblasts from patients with chronic periodontitis
复制标题
慢性牙周炎患者的牙龈组织和人牙龈成纤维细胞中保留了异常的线粒体结构和功能
DOI：
10.1111/jre.12941
复制
发表时间：
2021-11-26
影响因子：
3.5
通讯作者：
Luan, Qingxian
中科院分区：
文献类型：
--
作者：
Liu, Jia;Wang, Xiaoxuan;Luan, Qingxian
背景与目的细胞内线粒体结构和功能的异常与炎症性疾病密切相关。然而，慢性牙周炎（CP）患者牙龈组织和人牙龈成纤维细胞（HGFs）内线粒体的生理学尚不清楚。本研究的目的是探讨线粒体的结构和功能的牙龈组织和HGFs来自患者有或没有CP。进一步分析牙龈卟啉单胞菌脂多糖（LPS）诱导的HGFs中线粒体的这些特征。方法收集慢性前列腺炎患者和健康人的牙龈组织和牙龈成纤维细胞。线粒体结构通过透射电子显微镜进行评估。组织或细胞裂解进行线粒体DNA（mtDNA）定量，并使用实时聚合酶链反应（RT-PCR）测试来确定mtDNA拷贝数。蛋白质印迹分析用于评估自噬相关蛋白（ATG）-5，微管相关蛋白轻链3（LC 3）和线粒体基质蛋白丙酮酸脱氢酶激酶同工酶2（PDK 2）在CP和健康个体的组织和HGF中的水平。结果CP患者肝组织和HGF细胞线粒体结构破坏明显，线粒体DNA水平明显降低，ATG 5、LC 3-II水平明显升高，PDK 2蛋白水平明显降低。此外，来自P.g的LPS也在来自健康供体的HGF中引发相同的结果。此外，用LPS挑战来自CP的HGF使这些参数恶化。结论慢性牙周炎患者牙龈组织和牙龈成纤维细胞线粒体结构和功能均较正常人有明显的异常，脂多糖可促进线粒体的破坏。
Background and Objective The abnormal structure and function of mitochondria in cells is closely associated with inflammatory diseases. However, the physiology of mitochondria within gingival tissues and human gingival fibroblasts (HGFs) in patients with chronic periodontitis (CP) remains unclear. The objective of this study was to investigate the structure profile and function of mitochondria in gingival tissues and in HGFs derived from patients with or without CP. These features of mitochondria in HGFs were further analyzed when HGFs were induced by lipopolysaccharide (LPS) from Porphyromonas gingivalis (P.g). Methods Gingival tissues and HGFs were collected from CP and healthy patients. Mitochondrial structure was assessed by transmission electron microscopy. Tissues or cells lysis was performed for mitochondrial DNA (mtDNA) quantification, and real-time polymerase chain reaction (RT-PCR) tests were used to determine mtDNA copy numbers. Western blot analysis was used to evaluate autophagy-related protein (ATG)-5, microtubule-associated protein light chain 3 (LC3), and mitochondrial matrix protein pyruvate dehydrogenase kinase isozyme 2 (PDK2) levels in tissues and HGFs from CP and healthy individuals. Results Tissues and HGFs from CP showed a significant greater mitochondrial structure destruction, lower mtDNA level, increased ATG5, LC3-II, and lower PDK2 protein levels than those of healthy individuals. In addition, LPS from P.g also triggered the same results in HGFs from healthy donors. Moreover, the challenge of HGFs from CP with LPS worsened these parameters. Conclusion Mitochondrial structure and function within gingival tissues and HGFs from CP individuals were abnormal compared to those from healthy donors, and LPS could promote mitochondrial destruction.