Role of Smad4 from ocular surface ectoderm in retinal vasculature development
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Jing Li. Tianjin Eye Hospital, Tianjin Eye Institute, Tianjin Key Lab of Ophthalmology and Visual Science, Nankai University, Tianjin 300000, China. jingliwater123@163.com

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Supported by Tianjin Natural Science Funds (No.18JCQNJC10600).

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    Abstract:

    AIM: To investigate how signals from lens regulate retinal vascular development and neovascularization. METHODS: Le-Cre transgenic mouse line was employed to inactivate Smad4 in the surface ectoderm selectively. Standard histological and whole-mount retina staining were employed to reveal morphological changes of retinal vasculature in Smad4 defective eye. cDNA microarray and subsequent analyses were conducted to investigate the molecular mechanism underlying the vascular phenotype. Quantitative polymerase chain reaction (qPCR) was carried out to verify the microarrays results. RESULTS: We found that inactivation of Smad4 specifically on surface ectoderm leads to a variety of retinal vasculature anomalies. Microarray analyses and qPCR revealed that Sema3c, Sema3e, Nrp1, Tie1, Sox7, Sox17, and Sox18 are significantly affected in the knockout retinas at different developmental stages, suggesting that ocular surface ectoderm-derived Smad4 can signal to the retina and regulates various angiogenic signaling in the retina. CONCLUSION: Our data suggest that the cross-talk between ocular surface ectoderm and retina is important for retinal vasculature development, and Smad4 regulates various signaling associated with sprouting angiogenesis, vascular remodeling and maturation in the retina of mice.

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Li J, Zhang JS, Zhao JY, Han GG. Role of Smad4 from ocular surface ectoderm in retinal vasculature development. Int J Ophthalmol 2020;13(2):231-238

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History
  • Received:October 13,2019
  • Revised:December 09,2019
  • Adopted:
  • Online: February 03,2020
  • Published: