Mechanism of Proliferation of Cultured Human Corneal Endothelial Cells.
Mechanism of Proliferation of Cultured Human Corneal Endothelial Cells.
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DOI：
10.1097/ico.0000000000001337
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发表时间：
2017-11
期刊：
影响因子：
2.8
通讯作者：
T. Joko;A. Shiraishi;Takeshi Kobayashi;Y. Ohashi;S. Higashiyama
中科院分区：
文献类型：
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作者：
T. Joko;A. Shiraishi;Takeshi Kobayashi;Y. Ohashi;S. Higashiyama
因为人角膜内皮细胞（HCEC）一旦内皮单层形成就不增殖，所以角膜伤口愈合被认为是由细胞扩大或迁移介导的，而不是由增殖介导的。然而，HCEC参与伤口愈合的细胞机制尚未完全确定。本文综述了DNA结合转录因子-早幼粒细胞白血病锌指（PLZF）和转化生长因子β 2（TGF-β2）对体外培养的HCECs增殖和迁移的影响。还研究了丝裂原活化蛋白激酶（MAPK）信号通路在HCECs迁移中的作用。PLZF mRNA的表达随着细胞-细胞接触被破坏而降低，并且随着细胞-细胞接触重新形成而恢复到原始水平。实时细胞电子传感系统检测结果显示，Ad-PLZF感染和TGF-β2作用后，HCECs的增殖受到抑制。TGF-β2可通过激活p38 MAPK促进HCECs的迁移。我们的结论是，PLZF在培养的HCECs中的表达与细胞-细胞接触的形成密切相关，TGF-β2抑制培养的HCECs的增殖，同时通过p38 MAPK激活促进其迁移。
Because human corneal endothelial cells (HCECs) do not proliferate once the endothelial monolayer has formed, corneal wound healing is believed to be mediated by cell enlargement or migration, rather than by proliferation. However, the cellular mechanisms involved in wound healing by HCECs have not been fully determined. In this review, we focus on the effects of promyelocytic leukemia zinc finger (PLZF), a DNA-binding transcription factor, and transforming growth factor (TGF)-β2 on the proliferation and migration of cultured HCECs. Involvement of the mitogen-activated protein kinase (MAPK) signaling pathway in the migration of HCECs was also investigated. Expression of PLZF mRNA decreased as cell-cell contact was disrupted and returned to the original level as cell-cell contact was re-formed. Assessment with a real-time cell electronic sensing system revealed that proliferation of cultured HCECs was inhibited after infection with Ad-PLZF and exposure to TGF-β2. Migration of cultured HCECs was increased by TGF-β2 through p38 MAPK activation. We conclude that PLZF expression in cultured HCECs is closely related to the formation of cell-cell contact and that TGF-β2 suppresses proliferation of cultured HCECs, while promoting their migration through p38 MAPK activation.