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K. Terai, J. Yamada, S. Kinoshita; The Effect of TGF-β Signal Control on Mouse Corneal Endothelial Cell Proliferation. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3961.
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To confirm the effect of TGF-β signal control on damaged mouse corneal endothelial cell proliferation.
Eight-week-old C57/BL6 mice were anesthetized and their corneal endothelial cells were damaged by intracameral injection of 0.05% benzalkonium chloride for 15 seconds. In addition, in the transforming growth factor-beta (TGF-β) signal inhibition group, mice were treated by intracameral injection of 10 ug/mL TGF-β receptor-1 kinase inhibitor (CALBIOCHEM; EMD Chemicals, Inc., San Diego, CA). At various time-points after treatment, pictures of anterior segments of the eyes of the mice in each group were taken. Mice were sacrificed 2 hours after intraperitoneal injection of Bromodeoxyuridine (BrdU). Whole eyeballs were fixed by paraform aldehyde and embedded in paraffin, and then thin-sliced sections were made. Those sections were used for Hemaoxylin-Eosin staining or immunostaining for various TGF-β signal mediators. Corneal buttons were stained by alizarin red or stained immunohistochemically by using anti-BrdU antibody.
Mice corneal endothelial cells disappeared almost entirely by benzalkonium chloride injection. Corneal endothelial cells appeared from 1 or 2 days after benzalkonium chloride injection, and the cell proliferation was up-regulated in the TGF-β signal inhibition group compared to the control group. In observation of the anterior segments of the eyes, corneal transparency was higher in the TGF-β signal inhibition group than in the control group at 7 and 14 days after benzalkonium chloride injection.
It was confirmed that the TGF-β signal inhibition promoted corneal endothelial cell proliferation in vivo.
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