Noggin overexpression inhibits eyelid opening by altering epidermal apoptosis and differentiation

The study demonstrated that overexpression of the BMP antagonist noggin in transgenic mice significantly inhibited eyelid opening by altering apoptosis and cell differentiation in the eyelid epithelium. Transgenic mice showed a delay in eyelid opening by an average of 20.5 days compared to wild-type mice, with reduced apoptosis and altered keratinocyte differentiation. This was associated with downregulation of apoptotic receptors (Fas, p55 kDa TNFR), Id3 protein, and keratinocyte differentiation markers (loricrin, involucrin). The findings suggested that BMP signaling played a crucial role in regulating genetic programs for eyelid opening and skin remodeling during eye morphogenesis.