Related Experiment Videos
TGFbeta2 in corneal morphogenesis during mouse embryonic development
1Department of Ophthalmology, University of Cincinnati, Cincinnati, Ohio, USA.
Abstract:
To examine the roles of TGFbeta isoforms on corneal morphogenesis, the eyes of mice that lack TGFbetas 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 TGFbeta2 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.
Insights
Transforming growth factor beta 2 (TGF-β2) is crucial for normal eye development. Its absence in mice leads to abnormal ocular morphogenesis, including thin corneas and Peters
Area of Science:
- Developmental Biology
- Ophthalmology
- Molecular Biology
Background:
- Transforming growth factor beta (TGF-β) isoforms play critical roles in embryonic development.
- The specific functions of TGF-β isoforms in corneal morphogenesis are not fully understood.
Purpose of the Study:
- To investigate the roles of TGF-β isoforms in mouse corneal morphogenesis.
- To analyze the effects of TGF-β deficiency on ocular development, cell behavior, and gene expression.
Main Methods:
- Analysis of ocular development in mice lacking specific TGF-β isoforms (Tgfb(-/-)) at various developmental stages.
- Assessment of cell proliferation, migration, and apoptosis.
- Evaluation of gene expression patterns for keratin 12, lumican, keratocan, and collagen I.
Main Results:
- Tgfb2(-/-) mice exhibited abnormal ocular morphogenesis: thin corneal stroma, absent corneal endothelium, cornea-lens fusion (Peters'-like anomaly), and vitreous hyaline cell accumulation.
- Reduced keratocyte numbers and extracellular matrix (ECM) components (lumican, keratocan, collagen I) were observed in Tgfb2(-/-) corneas.
- Cell proliferation and apoptosis were not significantly affected; keratin 12 expression remained normal, indicating intact epithelial differentiation. Delayed macrophage infiltration was noted.
Conclusions:
- TGF-β2 is essential for normal corneal stroma formation and endothelial development.
- Reduced ECM synthesis in Tgfb2(-/-) mice likely contributes to thinner stroma and decreased cell numbers.
- Dysfunctional macrophages may play a role in the vitreous abnormalities observed in Tgfb2(-/-) mice.