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A developmental defect in astrocytes inhibits programmed regression of the hyaloid vasculature in the mammalian eye

Previously we reported the novel observation that astrocytes ensheath the persistent hyaloid artery, both in the Nuc1 spontaneous mutant rat, and in human PFV (persistent fetal vasculature) disease (Developmental Dynamics 234:36–47, 2005). We now show that astrocytes isolated from both the optic ner...

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Published in:European journal of cell biology 2011-05, Vol.90 (5), p.440-448
Main Authors: Zhang, Cheng, Asnaghi, Laura, Gongora, Celine, Patek, Bonnie, Hose, Stacey, Ma, Bo, Fard, Masoud Aghsaei, Brako, Lawrence, Singh, Kamaljeet, Goldberg, Morton F., Handa, James T., Lo, Woo-Kuen, Eberhart, Charles G., Zigler, J. Samuel, Sinha, Debasish
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Language:English
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Summary:Previously we reported the novel observation that astrocytes ensheath the persistent hyaloid artery, both in the Nuc1 spontaneous mutant rat, and in human PFV (persistent fetal vasculature) disease (Developmental Dynamics 234:36–47, 2005). We now show that astrocytes isolated from both the optic nerve and retina of Nuc1 rats migrate faster than wild type astrocytes. Aquaporin 4 (AQP4), the major water channel in astrocytes, has been shown to be important in astrocyte migration. We demonstrate that AQP4 expression is elevated in the astrocytes in PFV conditions, and we hypothesize that this causes the cells to migrate abnormally into the vitreous where they ensheath the hyaloid artery. This abnormal association of astrocytes with the hyaloid artery may impede the normal macrophage-mediated remodeling and regression of the hyaloid system.
ISSN:0171-9335
1618-1298
DOI:10.1016/j.ejcb.2011.01.003