期刊
DEVELOPMENTAL BIOLOGY
卷 479, 期 -, 页码 11-22出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2021.06.010
关键词
Pdgfrb; Mural cells; Pericytes; Vascular smooth muscle cells; Zebrafish
资金
- Swedish Research Council [2015-00550]
- European Research Council [AdG294556]
- Leducq Foundation [14CVD02]
- Swedish Cancer Society [150,735]
- Knut and Alice Wallenberg Foundation [2015.0030]
- Scientific Research on Innovative Areas Fluorescence Live Imaging [22113009]
- ''Neuro-Vascular Wiring'' from Ministry of Education, Culture, Sports, Science, and Technology, Japan [22122003]
- Japan Society for the Promotion of Science [26893336, 19K23835, 25293050, 24370084, 26670107]
- Ministry of Health, Labour, and Welfare of Japan
- Japan Science and Technology Agency for Act-X [JPMJAX1912]
- Core Research for Evolutional Science and Technology (CREST) program of Japan Agency for Medical Research and Development (AMED)
- PRIME, AMED
- Takeda Science Foundation
- Naito Foundation
- Mochida Memorial Foundation
- Daiichi Sankyo Foundation of Life Science
- Medical Research Council [MR/J001457/1]
- National Heart, Lung, and Blood Institute (NHLBI/NIH)
- Grants-in-Aid for Scientific Research [19K23835, 26893336, 22122003, 26670107, 25293050] Funding Source: KAKEN
The study demonstrates that Pdgfrb signaling plays a critical role in mural cells in zebrafish, and its absence can lead to issues such as cranial hemorrhage and vessel dilation. Similar to mice, pdgfrb mutant zebrafish also show defects in the structure of glomerulus, but normal development of hepatic stellate cells.
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.
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