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PDLSCs 通过外泌体转导的 VEGF 调控牙周炎中牙周韧带的血管生成。

PDLSCs Regulate Angiogenesis of Periodontal Ligaments via VEGF Transferred by Exosomes in Periodontitis.

机构信息

Department of General Surgery, Tang Du Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, People's Republic of China.

Department of Stomatology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, People's Republic of China.

出版信息

Int J Med Sci. 2020 Feb 10;17(5):558-567. doi: 10.7150/ijms.40918. eCollection 2020.

DOI:10.7150/ijms.40918
PMID:32210705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7085218/
Abstract

Abnormal angiogenesis is one of the significant features in periodontitis leading to progressive inflammation, but angiogenic changes of periodontal ligaments under inflammatory condition were rarely reported. Periodontal ligament stem cells (PDLSCs) were a kind of dental stem cells associated with vascularization. Here we investigated the alteration of angiogenesis of periodontal ligament in periodontitis, and revealed an exosome-mediated pathway to support the effect of PDLSCs on angiogenic improvement. Vascular specific marker CD31 and VEGFA were found to be highly expressed in periodontal ligaments of periodontitis. The VEGFA expression was up-regulated in inflamed PDLSCs compared to control, meanwhile the tube formation of HUVECs was improved when co-cultured with inflamed PDLSCs. Exosomes secretion of PDSLCs was augmented by inflammation, and promoted angiogenesis of HUVECs, whereas blocking secretion of exosomes led to degenerated angiogenesis of HUVECs. Exosome-trasferred VEGFA was proven to be the crucial communicator between PDLSCs and HUVECs. Inflammation inhibited miR-17-5p expression of PDLSCs and relieved its target VEGFA. However, overexpression of miR-17-5p blocked the pro-angiogenic ability of inflamed PDLSCs. In conclusion, the findings indicated that vascularization of periodontal ligaments was enhanced, and inflammatory micro-environment of periodontitis facilitated pro-angiogenesis of PDLSCs through regulating exosome-mediated transfer of VEGFA, which was targeted by miR-17-5p.

摘要

异常的血管生成是牙周炎的一个重要特征，导致炎症的进行性发展，但牙周韧带在炎症状态下的血管生成变化很少有报道。牙周韧带干细胞（PDLSCs）是一种与血管生成相关的牙齿干细胞。在这里，我们研究了牙周炎中牙周韧带血管生成的变化，并揭示了一种外泌体介导的途径来支持 PDLSCs 对血管生成改善的作用。在牙周炎中，血管特异性标志物 CD31 和 VEGFA 被发现高度表达。与对照相比，炎症中 PDLSCs 的 VEGFA 表达上调，同时与炎症 PDLSCs 共培养时 HUVEC 的管形成得到改善。炎症增强了 PDLSCs 的外泌体分泌，并促进了 HUVEC 的血管生成，而阻断外泌体的分泌则导致 HUVEC 的血管生成退化。证明外泌体转移的 VEGFA 是 PDLSCs 和 HUVECs 之间的关键通讯者。炎症抑制了 PDLSCs 中 miR-17-5p 的表达，并减轻了其靶标 VEGFA。然而，miR-17-5p 的过表达阻断了炎症 PDLSCs 的促血管生成能力。总之，这些发现表明，牙周韧带的血管化增强了，牙周炎的炎症微环境通过调节外泌体介导的 VEGFA 转移促进了 PDLSCs 的促血管生成作用，而 miR-17-5p 是其靶标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0175/7085218/8f75c299010b/ijmsv17p0558g006.jpg
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