| First Author | Li H | Year | 2019 |
| Journal | iScience | Volume | 19 |
| Pages | 559-571 | PubMed ID | 31445376 |
| Mgi Jnum | J:309082 | Mgi Id | MGI:6756020 |
| Doi | 10.1016/j.isci.2019.08.009 | Citation | Li H, et al. (2019) RECK in Neural Precursor Cells Plays a Critical Role in Mouse Forebrain Angiogenesis. iScience 19:559-571 |
| abstractText | RECK in neural precursor cells (NPCs) was previously found to support Notch-dependent neurogenesis in mice. On the other hand, recent studies implicate RECK in endothelial cells (ECs) in WNT7-triggered canonical WNT signaling essential for brain angiogenesis. Here we report that RECK in NPCs is also critical for brain angiogenesis. When Reck is inactivated in Foxg1-positive NPCs, mice die shortly after birth with hemorrhage in the forebrain, with angiogenic sprouts stalling at the periphery and forming abnormal aggregates reminiscent of those in EC-selective Reck knockout mice and Wnt7a/b-deficient mice. The hemorrhage can be pharmacologically suppressed by lithium chloride. An effect of RECK in WNT7-producing cells to enhance canonical WNT-signaling in reporter cells is detectable in mixed culture but not with conditioned medium. Our findings suggest that NPC-expressed RECK has a non-cell-autonomous function to promote forebrain angiogenesis through contact-dependent enhancement of WNT signaling in ECs, implying possible involvement of RECK in neurovascular coupling. |
