Wang Yanli, Yang Congchong
Department of Stomatology, Xi'an Central Hospital, Xi'an, Shaanxi, China.
Department of Cariology and Endodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
J Dent Sci. 2022 Apr;17(2):876-881. doi: 10.1016/j.jds.2021.09.022. Epub 2021 Sep 25.
BACKGROUD/PURPOSE: The effects of inflammatory cytokines were reported to involve in the process of periodontal disease and inflamed tissue enhanced the expression of inflammatory mediators which in turn may promote angiogenesis. Human gingival fibroblasts (HGFs) exert the basic function in periodontal tissue repair and regeneration. However, studies specially focused on the effects of inflammation-related HGFs on angiogenic and osteogenic differentiation are limited. This study was aimed to test whether HGFs enhance vascular endothelial growth factor (VEGF)-A expression mediating angiogenic and osteogenic differentiation by stimulating with tumor necrosis factor-α (TNF-α), to further identify the possible mechanism which may be responsible for this activity.
In this study, HGFs are treated by TNF-α in order to detect the effects of angiogenic and osteogenic differentiation under inflammation-related condition.
TNF-α enhances VEGF-A expression and results in increasing cell migration and angiogenic differentiation and inhibiting osteogenic differentiation in HGFs. Besides, TNF-α stimulated VEGF-A-mediated angiogenic differentiation is dependent on the activation of mitogen-activated protein kinase (MAPK) pathway, Extracellular signal-regulated kinase (ERK) 1/2 phosphorylation may contribute to regulate the function of VEGF-A in inflammation-related HGFs.
This study demonstrated that enhanced VEGF-A-mediated angiogenic differentiation in HGFs is dependent on the activation of MAPK pathway by stimulating with TNF-α in vitro. Therefore, this study could provide better understand for the progression of inflammation-related periodontal diseases.
背景/目的:据报道,炎性细胞因子的作用涉及牙周疾病的进程,且炎症组织中炎性介质的表达增强,这反过来可能促进血管生成。人牙龈成纤维细胞(HGFs)在牙周组织修复和再生中发挥基本功能。然而,专门聚焦于炎症相关的HGFs对血管生成和骨生成分化影响的研究有限。本研究旨在检测HGFs是否通过肿瘤坏死因子-α(TNF-α)刺激增强血管内皮生长因子(VEGF)-A表达,介导血管生成和骨生成分化,以进一步确定可能负责此活性的潜在机制。
在本研究中,用TNF-α处理HGFs,以检测炎症相关条件下血管生成和骨生成分化的影响。
TNF-α增强VEGF-A表达,导致HGFs中细胞迁移增加和血管生成分化增加,并抑制骨生成分化。此外,TNF-α刺激的VEGF-A介导的血管生成分化依赖于丝裂原活化蛋白激酶(MAPK)途径的激活,细胞外信号调节激酶(ERK)1/2磷酸化可能有助于调节炎症相关HGFs中VEGF-A的功能。
本研究表明,体外通过TNF-α刺激,HGFs中增强的VEGF-A介导的血管生成分化依赖于MAPK途径的激活。因此,本研究可为炎症相关牙周疾病的进展提供更好的理解。