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Ninjurin1 mediates macrophage-induced programmed cell death during early ocular development

Cited 49 time in Web of Science Cited 52 time in Scopus
Authors
Lee, H-J; Ahn, B. J.; Shin, M. W.; Jeong, J-W; Kim, K-W; Kim, J. H.
Issue Date
2009-10
Publisher
NATURE PUBLISHING GROUP
Citation
CELL DEATH AND DIFFERENTIATION; Vol.16 10; 1395-1407
Keywords
vascular biologycell adhesionmacrophageNinjurin1apoptosis
Abstract
Developmental tissues go through regression, remodeling, and apoptosis. In these processes, macrophages phagocytize dead cells and induce apoptosis directly. In hyaloid vascular system (HVS), macrophages induce apoptosis of vascular endothelial cells (VECs) by cooperation between the Wnt and angiopoietin (Ang) pathways through cell-cell interaction. However, it remains unclear how macrophages are activated and interact with VECs. Here we show that Ninjurin1 (nerve injury-induced protein; Ninj1) was temporally increased in macrophages during regression of HVS and these Ninj1-expressing macrophages closely interacted with hyaloid VECs. Systemic neutralization using an anti-Ninj1 antibody resulted in the delay of HVS regression in vivo. We also found that Ninj1 increased cell-cell and cell-matrix adhesion of macrophages. Furthermore, Ninj1 stimulated the expression of Wnt7b in macrophages and the conditioned media from Ninj1-overexpressing macrophages (Ninj1-CM) decreased Ang1 and increased Ang2 in pericytes, which consequently switched hyaloid VEC fate from survival to death. Collectively, these findings suggest that macrophages express Ninj1 to increase the death signal through cell-cell interaction and raise the possibility that Ninj1 may act similarly in other developmental regression mediated by macrophages.
ISSN
1350-9047
Language
English
URI
https://hdl.handle.net/10371/77963
DOI
https://doi.org/10.1038/cdd.2009.78
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College of Medicine/School of Medicine (의과대학/대학원)Ophthalmology (안과학전공)Journal Papers (저널논문_안과학전공)
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