Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/110295
Title: Tafazzin regulates human conjunctiva epithelial cell proliferation via inhibiting TGFβ signaling pathway
Authors: Tan, X.W.
Beuerman, R.W.
Poh, C.K.
Mehta, J.S. 
Issue Date: 1-Jun-2012
Citation: Tan, X.W.,Beuerman, R.W.,Poh, C.K.,Mehta, J.S. (2012-06-01). Tafazzin regulates human conjunctiva epithelial cell proliferation via inhibiting TGFβ signaling pathway. Molecular Vision 18 : 1402-1410. ScholarBank@NUS Repository.
Abstract: Purpose: To investigate the role of Tafazzin (TAZ) protein in regulating the proliferation of normal human conjunctiva epithelial cells and epithelial cells from pterygium tissue. Methods: Conjunctiva epithelial cells were cultured in keratinocytes growth medium and treated with transformation growth factor β (TGFβ) to analyze the expression and translocation of TAZ protein by immunostaining and BrdU analysis. Immortalized conjunctiva epithelial cells (NHC) were treated with TGFβ, targeting siRNA, TGFβ receptor antibody or TGFβ receptor inhibitor, to study the involvement of TAZ and TGFβ signaling pathway in conjunctiva cell proliferation by cell adhesion assay. Conjunctiva tissues from a normal human eye and an eye with pterygium disease were collected for histological analyses and western blot to evaluate the TAZ protein expression in vivo. Results: TAZ expression was upregulated in mitotic conjunctiva epithelial cells, proliferating conjunctiva epithelial cells, TGFβ treated conjunctiva epithelial cells and human pterygium epithelium. TAZ siRNA induced less conjunctiva epithelial cell growth. Moreover, TGFβ receptor antibody and TGFβ receptor inhibitor rescued this anti-proliferative effect of TAZ siRNA. Conclusions: TAZ is involved in human conjunctiva epithelial cells proliferation via regulating TGFβ signaling pathway. © 2012 Molecular Vision.
Source Title: Molecular Vision
URI: http://scholarbank.nus.edu.sg/handle/10635/110295
ISSN: 10900535
Appears in Collections:Staff Publications

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