磷脂酶C-β3信号通路对视网膜血管生成的调控
Regulation of retinal angiogenesis by phospholipase C-β3 signaling pathway.
作者信息
Ha Jung Min, Baek Seung Hoon, Kim Young Hwan, Jin Seo Yeon, Lee Hye Sun, Kim Sun Ja, Shin Hwa Kyoung, Lee Dong Hyung, Song Sang Heon, Kim Chi Dae, Bae Sun Sik
机构信息
Department of Pharmacology, Gene and Cell Therapy Center for Vessel-Associated Disease, Medical Research Institute, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Department of Anesthesia and Pain Medicine, Pusan National University Hospital, Yangsan, Republic of Korea.
出版信息
Exp Mol Med. 2016 Jun 17;48(6):e240. doi: 10.1038/emm.2016.39.
Angiogenesis has an essential role in many pathophysiologies. Here, we show that phospholipase C-β3 (PLC-β3) isoform regulates endothelial cell function and retinal angiogenesis. Silencing of PLC-β3 in human umbilical vein endothelial cells (HUVECs) significantly delayed proliferation, migration and capillary-like tube formation. In addition, mice lacking PLC-β3 showed impaired retinal angiogenesis with delayed endothelial proliferation, reduced endothelial cell activation, abnormal vessel formation and hemorrhage. Finally, tumor formation was significantly reduced in mice lacking PLC-β3 and showed irregular size and shape of blood vessels. These results suggest that regulation of endothelial function by PLC-β3 may contribute to angiogenesis.
血管生成在许多病理生理过程中起着至关重要的作用。在此，我们表明磷脂酶C-β3（PLC-β3）亚型调节内皮细胞功能和视网膜血管生成。在人脐静脉内皮细胞（HUVECs）中沉默PLC-β3可显著延迟细胞增殖、迁移和毛细血管样管形成。此外，缺乏PLC-β3的小鼠表现出视网膜血管生成受损，内皮细胞增殖延迟，内皮细胞活化减少，血管形成异常和出血。最后，缺乏PLC-β3的小鼠肿瘤形成显著减少，且血管大小和形状不规则。这些结果表明，PLC-β3对内皮功能的调节可能有助于血管生成。
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