Inactivation of Smad4 leads to impaired ocular development and cataract formation

Ying Liu, Kirio Kawai, Shabnam Khashabi, Chuxia Deng, Yi Hsin Liu, Samuel Yiu

Research output: Contribution to journalArticlepeer-review

Abstract

Purpose: Signaling by members of the TGFβ superfamily of molecules is essential for embryonic development and homeostasis. Smad4, a key intracellular mediator in TGFβ signaling, forms transcriptional activator complexes with Activin-, BMP-, and TGFβ-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.

Original languageEnglish (US)
Pages (from-to)476-482
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume400
Issue number4
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

Keywords

  • Eyelid closure failure
  • Lens
  • Ocular development
  • Smad4

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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