[The mechanism of twist gene regulation during the retina angiogenesis].
OBJECTIVE
To study the mechanisms of the Twist gene and cell transition during the angiogenesis in a mouse model of oxygen induced retinopathy.


METHODS
It was a experimental study. 40 new born C57/BL mice were divided into two groups; the control group, which were fed in the room air, and the study group, which were fed 7 days in the normal environment, followed by exposure to hyperoxia (75% O2) for 5 days. The mice were sacrificed at post born 12 day and post born 17 day. The Twist and VE-cadherin expression were detected with immunohistochemistry. The total retinal RNA was extracted and the expression level of the VE-cadherin, vimentin and twist were examined with RT-PCR method.


RESULTS
Immunohistochemistry proved there was no significant difference at post born 12 day. At post born 17 day, compared with the control group (75.36 +/- 7.04),VE-cadherin expression of hyperoxia group (65.19 +/- 8.39) decreased (F =8.616, P =0.009). Compared with the control group (82.14 +/- 6.32), Vimentin expression of hyperoxia group (95.09 +/- 14.13) increased, compared with the control group (93.30 +/- 6.37), Twist expression of hyperoxia group (119.48 +/- 7.90) increased (F = 66.557, P = 0.000) significantly. RT-PCR examination revealed there exist the interaction between Vimentin, Twist expression and the detection time (F = 5.508, P = 0.032; F = 17.760, P = 0.001; respectively). At post born 12 day, compared with the control group (0.77 +/- 0.10), VE-cadherin expression of hyperoxia group (0.64 +/- 0.09) decreased (P = 0.047). Compared with the control group (0.24 +/- 0.05), Vimentin expression of hyperoxia group (0.39 +/- 0.09) increased (P = 0.033). At post born 17 day, compared with the control group (0.75 +/- 0.12), VE-cadherin expression of hyperoxia group (0.51 +/- 0.07) decreased more obviously (P = 0.002), compared with the control group (0.36 +/- 0.06), Vimentin expression of hyperoxia group (0.70 +/- 0.14) increased (P = 0.000). Compared with the control group(0.89 +/- 0.11), Twist expression of hyperoxia group (1.24 +/- 0.15) increased (P = 0.003).


CONCLUSIONS
Twist, as a cell transition gene, participated in the angiogenesis of the oxygen induced retinopathy, and that the Twist induced endothelium-mesenchymal transition may be one of the main reasons.
Liu
Ting
T
State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Qingdao, China.
Dong
Xiao-Guang
XG
Wang
Yao
Y
Yan
Yan
Y
Zhang
Jing-Jing
JJ
D000818:Animals; D015703:Antigens, CD / Q000235:genetics; D015820:Cadherins / Q000235:genetics; D002454:Cell Differentiation; D004730:Endothelium, Vascular / Q000166:cytology; D005786:Gene Expression Regulation; D018496:Hyperoxia / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D009687:Nuclear Proteins / Q000235:genetics*; D015861:Retinal Neovascularization / Q000235:genetics* / Q000473:pathology; D051879:Twist-Related Protein 1 / Q000235:genetics*; D014746:Vimentin / Q000235:genetics; D000099152:Cadherin 5
D015703:Antigens, CD; D015820:Cadherins; D009687:Nuclear Proteins; D051879:Twist-Related Protein 1; D014746:Vimentin; D000099152:Cadherin 5; C067250:Twist1 protein, mouse