Abstract
Purpose: :
Cornea is well-known as an organ which is devoid of blood and lymphatic vessels at the adult age. Mouse cornea has been widely used for vascular studies. However, it still remains unknown whether the avascularity of mouse cornea is the result of complete absence of vessel formation throughout the developmental stages or subsequent induction of vessel regression at a certain period of embryogenesis, which is the major focus of this study.
Methods: :
Normal C57BL/6 mouse eyeballs were sampled on embryonic day (E)10.5, 11.5, 13.5, 14.5, 16.5, 18.5, postnatal day (P) 2, 7, 14, and at 6 weeks. Cryosections were investigated by light, deconvolutional fluorescent, and confocal microscopic studies using specific antibodies against LYVE-1 (a lymphatic specific marker) and CD31 (a panendothelial marker).
Results: :
LYVE-1 or CD31 expression was not detected in the mouse cornea at all time points studied. In contrast, LYVE-1 positive cells were observed in mouse eyelids at E13.5 and thereafter.
Conclusions: :
In this study, we provide the first evidence that mouse cornea maintains its avascularity throughout the embryonic and postnatal stages. This avascularity is not derived from regression of preformed vessels. Our results are consistent with a recent report on human cornea, further confirming the similarity between mouse and human corneas from early embryonic to adult stages. However, the mechanism by which cornea maintains its avascularity throughout the entire development process is still unknown. Unlike human studies which are largely hampered by ethnic issues and subject availability, our future mouse studies can take the great advantage of various transgenic, knockout, or disease models to advance our knowledge in this field.
Keywords: neovascularization • development • microscopy: light/fluorescence/immunohistochemistry