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[Effects of endostatin on the expression of Tubulinbeta mRNA in the retina of oxygen-induced retinal neovascularization].

AbstractOBJECTIVE:
To investigate the effect of endostatin on the expression of Tubulinbeta in the retina of oxygen-induced retinal neovascularization.
METHODS:
Fifty four one-week-old C57 BL/6 mice were randomly and evenly divided into three groups: which were Control group, Hyperoxia group, and endostatin (ES) treated hyperoxia group. In control group, the mice were bred in normal oxygen condition, while the mice in another 2 groups were subjected to hyperoxia condition to establish the oxygen-induced retinal neovascularization model. In ES treated group, 1 microL endostatin (1 microg/microL) were injected into one side of vitreous 12 h, 36 h after the mice were removed out from the oxygen box. Total RNA were extracted from retina of each mouse in three groups, the quantity of Tubulinbeta mRNA in retina was analyzed with quantitative real-time PCR with the special primers.
RESULTS:
Quantitativereal-time PCR results indicated that, the expression of Tubulinbeta mRNA in retica was up-regulated in the process of retinal neovascularization induced by hyperoxia, and down-regulated by the treatment of ES.
CONCLUSIONS:
Endotatin can inhibit the expression of Tubulinbeta mRNA in retinal neovascularization, this may be correlated with the inhibitive characteristics of ES on neovascularization.
AuthorsLing Duan, Mei-Xia Zhang
JournalSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition (Sichuan Da Xue Xue Bao Yi Xue Ban) Vol. 40 Issue 6 Pg. 1008-10, 1020 (Nov 2009) ISSN: 1672-173X [Print] China
PMID20067108 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Endostatins
  • RNA, Messenger
  • Tubulin
  • beta3 tubulin, mouse
Topics
  • Animals
  • Animals, Newborn
  • Endostatins (pharmacology)
  • Hyperoxia (metabolism)
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger (genetics, metabolism)
  • Random Allocation
  • Retina (metabolism)
  • Retinal Neovascularization (chemically induced, metabolism)
  • Tubulin (genetics, metabolism)

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