Regulation of retinal angiogenesis by phospholipase C-β3 signaling pathway

被引:9
作者
Ha, Jung Min [1 ]
Baek, Seung Hoon [2 ]
Kim, Young Hwan [1 ]
Jin, Seo Yeon [1 ]
Lee, Hye Sun [1 ]
Kim, Sun Ja [3 ]
Shin, Hwa Kyoung [4 ]
Lee, Dong Hyung [5 ]
Song, Sang Heon [6 ]
Kim, Chi Dae [1 ]
Bae, Sun Sik [1 ]
机构
[1] Pusan Natl Univ, Sch Med, Gene & Cell Therapy Ctr Vessel Associated Dis, Dept Pharmacol,Med Res Inst, Yangsan, South Korea
[2] Pusan Natl Univ Hosp, Dept Anesthesia & Pain Med, Yangsan, South Korea
[3] Dong A Univ, Dept Phys, Busan, South Korea
[4] Pusan Natl Univ Korean Med, Dept Anat, Yangsan, South Korea
[5] Pusan Natl Univ Hosp, Dept Obstet & Gynecol, Yangsan, South Korea
[6] Pusan Natl Univ Hosp, Dept Internal Med, Busan, South Korea
基金
新加坡国家研究基金会;
关键词
VEGF-MEDIATED ANGIOGENESIS; ENDOTHELIAL GROWTH-FACTOR; VASCULAR DEVELOPMENT; C ISOZYMES; IN-VITRO; PDGF-B; CELLS; MORPHOGENESIS; ACTIVATION; EXPRESSION;
D O I
10.1038/emm.2016.39
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Angiogenesis has an essential role in many pathophysiologies. Here, we show that phospholipase C-beta 3 (PLC-beta 3) isoform regulates endothelial cell function and retinal angiogenesis. Silencing of PLC-beta 3 in human umbilical vein endothelial cells (HUVECs) significantly delayed proliferation, migration and capillary-like tube formation. In addition, mice lacking PLC-beta 3 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-beta 3 and showed irregular size and shape of blood vessels. These results suggest that regulation of endothelial function by PLC-beta 3 may contribute to angiogenesis.
引用
收藏
页码:e240 / e240
页数:8
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