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Mitochondrial profile and responses to TGF-? ligands in Keratoconus #MMPMID26430764
Sarker-Nag A; Hutcheon AEK; Karamichos D
Curr Eye Res 2016[Jul]; 41 (7): 900-7 PMID26430764show ga
PURPOSE: Keratoconus (KC) is a complex corneal dystrophy with multifactorial etiology. Previous studies have shown evidence of mitochondrial abnormalities in KC; however, the exact cause of these abnormalities remains unknown. The aim of this study was to identify if transforming growth factor-? (TGF-?) isoforms play a role in the regulation of mitochondrial proteins in human keratoconus cells (HKC). MATERIALS AND METHODS: Human corneal fibroblasts (HCF) and HKC were isolated and cultured for four weeks in three different conditions: a) Control: MEM+10%FBS, b) MEM+10%FBS+TGF-?1, and c) MEM+10%FBS+TGF-?3. All samples were processed for mitochondrial damage analysis using real-time PCR. RESULTS: We quantified and analyzed 84 mitochondrial and 5 housekeeping genes in HCFs and HKCs. Our data showed that when TGF-?1 and/or TGF-?3 were compared with control in HCFs, nine genes were significantly different; however, no genes were significantly regulated by the TGF-? isoforms in HKCs. Significant differences were also seen in seven genes when HFCs were compared to HKCs, in all three conditions. CONCLUSIONS: Overall, our data supports the growing consensus that mitochondrial dysfunction is a key player in KC disease. These in vitro data show clear links between mitochondrial function and TGF-? isoforms, with TGF-?1 severely disrupting KC-mitochondrial function, while TGF-?3 maintained it, thus suggesting that TGF-? may play a role in KC-disease treatment.
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Curr+Eye+Res 2016 ; 41 (7): 900-7
