Abstract
Purpose: :
To investigate the effect of 1, 25-Dihydroxyvitamin D3 (1,25(OH)2D3) on expression of transforming growth factor-beta induced gene protein (TGFBIp) in normal human corneal epithelial cells (HCE), normal human corneal fibroblasts (HCF) and homozygote granular corneal dystrophy type 2 (GCD2) corneal fibroblasts.
Methods: :
Cultured HCE, HCF and homozygote GCD2 HCF were treated with various concentration and time of vitamin D3. The levels of expression of TGFBIp and Smad phosphorylation were analyzed by immunoblotting and the levels of TGFBI mRNA was analyzed by RT-PCR.
Results: :
The expressions of TGFBIp and its mRNA of HCE, HCF and GCD2 homozygous fibroblasts were decreased by vitamin D3 in dose- and time-dependent manner. Furthermore, vitamin D3 suppressed expression of TGFBIp and the Smad3 phosphorylation induced by TGF-β1. These effects of vitamin D3 were attenuated in the vitamin D receptor (VDR)-knock down corneal epithelial cells and fibroblasts. Cell viability analysis at different doses was greater than 90%, demonstrating that vitamin D3 did not inhibit prolieration of corneal epithelial and fibroblasts.
Conclusions: :
Vitmain D3 reduces the expression of TGFBI mRNA and TGFBIp in HCE, HCF and homozygote GCD2 HCF via VDR. These data suggest that vitamin D3 might be an ancillary treatment modality of GCD2 and other TGFBI-related corneal dystrophies.
Keywords: cornea: basic science • cornea: stroma and keratocytes • cornea: epithelium