Tgfβ2 in corneal morphogenesis during mouse embryonic development

Shizuya Saika, Satoko Saika, Chia Yang Liu, Mohamad Azhar, L. Philip Sanford, Thomas Doetschman, Robert L. Gendron, Candace W.C. Kao, Winston W.Y. Kao

Research output: Contribution to journalArticlepeer-review

141 Scopus citations


To examine the roles of TGFβ isoforms on corneal morphogenesis, the eyes of mice that lack TGFβs were analyzed at different developmental stages for cell proliferation, migration and apoptosis, and for expression patterns of keratin 12, lumican, keratocan and collagen I. Among the three Tgfb-/- mice, only Tgfb2-/- mice have abnormal ocular morphogenesis characterized by thin corneal stroma, absence of corneal endothelium, fusion of cornea to lens (a Peters'-like anomaly phenotype), and accumulation of hyaline cells in vitreous. In Tgfb2-/- mice, fewer keratocytes were found in stroma that has a decreased accumulation of ECM; for example, lumican, keratocan and collagen I were greatly diminished. The absence of TGFβ2 did not compromise cell proliferation, nor enhance apoptosis. The thinner stroma resulting from decreased ECM synthesis may account for the decreased cell number in the stroma of Tgfb2 null mice. Keratin 12 expression was not altered in Tgfb2-/- mice, implicating normal corneal type epithelial differentiation. Delayed appearance of macrophages in ocular tissues was observed in Tgfb2-/- mice. Malfunctioning macrophages may account for accumulation of cell mass in vitreous of Tgfb2 null mice.

Original languageEnglish (US)
Pages (from-to)419-432
Number of pages14
JournalDevelopmental biology
Issue number2
StatePublished - Dec 15 2001


  • Collagen I
  • Cornea
  • Development
  • Extracellular matrix
  • Gene targeting
  • Keratin 12
  • Keratocan
  • Knockout mice
  • Lumican

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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