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Anat Embryol (Berl). 1999 Oct;200(4):403-11.

Regression of the hyaloid vessels and pupillary membrane of the mouse.

Author information

1
Department of Anatomy, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan. QZA04257@nifty.ne.jp

Abstract

Regression of the pupillary membrane (PM) and hyaloid vessels - hyaloid arteries (HAs), tunica vasculosa lentis (TVL), and vasa hyaloidea propria (VHP) - in mice aged from 0 to 16 days was observed using stereomicroscopy and transmission electron microscopy. Whole-mount stereomicroscopy revealed that the pattern of normal developed vessels was basically the same as that reported in rats and rabbits and that the VHP and PM disappeared between 12 and 16 days and 10 and 12 days, respectively, while certain examples of the TVL and HA remained even at 16 days. In the TVL, VHP and PM, regression occurred segmentally and resulted in a decreased number of interconnections. The ultrastructure of the vessels in the VHP, TVL and PM was consistent with a typical capillary with pericyte covering and no fenestrations. HAs had tunica media and adventitia in the older stages. Some endothelial cells in the TVL and PM attaching to the lens capsule were thin at the side of the lens. Many macrophages were observed in the vitreous and around vessels in the whole-mount specimens at all stages. Some macrophages remained linearly arranged even after vessels became vestigial and disappeared. In transmission electron microscopy, most of these macrophages were seen to possess vacuoles and/or processes, and some of them had phagosomes. Electron microscopic findings from regressing ocular vessels were consistent with the apoptosis of both endothelia and pericytes. Obstruction of the vessels was noted at older stages. These results add further anatomical information to previous studies and suggest that the VHP and TVL as well as PM regress via apoptosis. The precise mechanisms of regression of hyaloid vessels and the role of macrophages remain for further studies.

PMID:
10460477
DOI:
10.1007/s004290050289
[Indexed for MEDLINE]

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