| First Author | Liu Y | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 400 |
| Issue | 4 | Pages | 476-82 |
| PubMed ID | 20735985 | Mgi Jnum | J:165593 |
| Mgi Id | MGI:4837794 | Doi | 10.1016/j.bbrc.2010.08.065 |
| Citation | Liu Y, et al. (2010) Inactivation of Smad4 leads to impaired ocular development and cataract formation. Biochem Biophys Res Commun 400(4):476-82 |
| abstractText | PURPOSE: Signaling by members of the TGFbeta superfamily of molecules is essential for embryonic development and homeostasis. Smad4, a key intracellular mediator in TGFbeta signaling, forms transcriptional activator complexes with Activin-, BMP-, and TGFbeta-restricted Smad proteins. However, the functional role of Smad4 in controlling different visual system compartments has not been fully investigated. METHODS: Using the Pax6 promoter-driven Cre transgenic, smad4 was conditionally inactivated in the lens, cornea and ectoderm of the eyelids. Standard histological and molecular analytical approaches were employed to reveal morphological and cellular changes. RESULTS: Inactivation of Smad4 in the lens led to microphthalmia and cataract formation in addition to the persistent adhesion of the retina to the lens and the iris to the cornea. Inactivation of Smad4 from the ectoderm of the eyelid and cornea caused disruption to eyelid fusion and proper development of the corneal epithelium and corneal stroma. CONCLUSIONS: Smad4 is required for the development and maintenance of the lens in addition to the proper development of the cornea, eyelids, and retina. |
