“…A single injection of TGF-β into the vitreous body of rats causes a loss of lens transparency, and it has been suggested that intraocular administration of TGF-β could contribute to the very rapid progression of cataracts in human patients undergoing treatment to heal macular holes ( Thompson et al , 1995 ; Hales et al , 1999 ; Robertson et al , 2007 ). Moreover, several conditions associated with an increase in the levels of active TGF-β in the lens environment (e.g., diabetes, glaucoma, atypical retinoblastoma) have been linked to higher rates of cataract formation in humans ( Harding et al , 1993 ; Klein et al , 1998 ; Ochiai and Ochiai, 2002 ; Kase et al , 2008 ), as has a decrease in an anti-TGF-β defense system, estrogen ( Klein et al , 1994 ; Benitez del Castillo et al , 1997 ; Hales et al , 1997 ; Freeman et al , 2001 ). Because of the role of TGF-β in lens pathology and the importance of gap junctions to normal lens function, we examined if TGF-β affects lens cell GJIC in either the absence or presence of physiologically relevant concentrations of FGF.…”