Conserved and context-dependent roles for pdgfrb signaling during zebrafish vascular mural cell development.

Autor:	Ando K; Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Dag Hammarskjölds Väg 20, SE-751 85, Uppsala, Sweden; Department of Molecular Pathophysiology, Institute of Advanced Medical Sciences, Nippon Medical School, Sendagi Bunkyo-ku, Tokyo, 113 8602, Japan. Electronic address: koji-ando@nms.ac.jp., Shih YH; Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, 01650, United States., Ebarasi L; Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Stockholm, Sweden., Grosse A; Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, 01650, United States., Portman D; Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, 01650, United States., Chiba A; Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, 564 8565, Japan., Mattonet K; Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Ludwigstrasse 43, 61231, Bad Nauheim, Germany., Gerri C; Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Ludwigstrasse 43, 61231, Bad Nauheim, Germany; Human Embryo and Stem Cell Laboratory, The Francis Crick Institute, 1 Midland Road, London, NW1 1AT, UK., Stainier DYR; Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Ludwigstrasse 43, 61231, Bad Nauheim, Germany., Mochizuki N; Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, 564 8565, Japan., Fukuhara S; Department of Molecular Pathophysiology, Institute of Advanced Medical Sciences, Nippon Medical School, Sendagi Bunkyo-ku, Tokyo, 113 8602, Japan., Betsholtz C; Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Dag Hammarskjölds Väg 20, SE-751 85, Uppsala, Sweden; Department of Medicine Huddinge (MedH), Karolinska Institutet, Campus Flemingsberg, Neo, Blickagången 16, Hiss S, Plan 7, SE-141 57, Huddinge, Sweden., Lawson ND; Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, 01650, United States. Electronic address: nathan.lawson@umassmed.edu.
Jazyk:	angličtina
Zdroj:	Developmental biology [Dev Biol] 2021 Nov; Vol. 479, pp. 11-22. Date of Electronic Publication: 2021 Jul 24.
DOI:	10.1016/j.ydbio.2021.06.010
Abstrakt:	Platelet derived growth factor beta and its receptor, Pdgfrb, play essential roles in the development of vascular mural cells, including pericytes and vascular smooth muscle cells. To determine if this role was conserved in zebrafish, we analyzed pdgfb and pdgfrb mutant lines. Similar to mouse, pdgfb and pdgfrb mutant zebrafish lack brain pericytes and exhibit anatomically selective loss of vascular smooth muscle coverage. Despite these defects, pdgfrb mutant zebrafish did not otherwise exhibit circulatory defects at larval stages. However, beginning at juvenile stages, we observed severe cranial hemorrhage and vessel dilation associated with loss of pericytes and vascular smooth muscle cells in pdgfrb mutants. Similar to mouse, pdgfrb mutant zebrafish also displayed structural defects in the glomerulus, but normal development of hepatic stellate cells. We also noted defective mural cell investment on coronary vessels with concomitant defects in their development. Together, our studies support a conserved requirement for Pdgfrb signaling in mural cells. In addition, these zebrafish mutants provide an important model for definitive investigation of mural cells during early embryonic stages without confounding secondary effects from circulatory defects. Competing Interests: Declaration of competing interest The authors declare no competing or financial interests. (Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
Externí odkaz:	Full Text from ScienceDirect