Akt3 activation by R-Ras in an endothelial cell enforces quiescence and barrier stability of neighboring endothelial cells via Jagged1.
| Autor: | Herrera JL; Cancer and Blood Disorders Institute, Institute for Fundamental Biomedical Research, and Department of Surgery, Johns Hopkins All Children's Hospital, St. Petersburg, FL 33701, USA; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA., Komatsu M; Cancer and Blood Disorders Institute, Institute for Fundamental Biomedical Research, and Department of Surgery, Johns Hopkins All Children's Hospital, St. Petersburg, FL 33701, USA; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Electronic address: mkomats1@jhmi.edu. |
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| Jazyk: | angličtina |
| Zdroj: | Cell reports [Cell Rep] 2024 Mar 26; Vol. 43 (3), pp. 113837. Date of Electronic Publication: 2024 Feb 24. |
| DOI: | 10.1016/j.celrep.2024.113837 |
| Abstrakt: | Communication between adjacent endothelial cells is important for the homeostasis of blood vessels. We show that quiescent endothelial cells use Jagged1 to instruct neighboring endothelial cells to assume a quiescent phenotype and secure the endothelial barrier. This phenotype enforcement by neighboring cells is operated by R-Ras through activation of Akt3, which results in upregulation of a Notch ligand Jagged1 and consequential upregulation of Notch target genes, such as UNC5B, and VE-cadherin accumulation in the neighboring cells. These signaling events lead to the stable interaction between neighboring endothelial cells to continue to fortify juxtacrine signaling via Jagged1-Notch. This mode of intercellular signaling provides a positive feedback regulation of endothelial cell-cell interactions and cellular quiescence required for the stabilization of the endothelium. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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