@article{8a4c173f4ad546ac9603261e3869a87a,
title = "Tissue Myeloid Progenitors Differentiate into Pericytes through TGF-β Signaling in Developing Skin Vasculature",
abstract = "Mural cells (pericytes and vascular smooth muscle cells) are essential for the regulation of vascular networks and maintenance of vascular integrity, but their origins are diverse in different tissues and not known in the organs that arise from the ectoderm, such as skin. Here, we show that tissue-localized myeloid progenitors contribute to pericyte development in embryonic skin vasculature. A series of in vivo fate-mapping experiments indicates that tissue myeloid progenitors differentiate into pericytes. Furthermore, depletion of tissue myeloid cells and their progenitors in PU.1 (also known as Spi1) mutants results in defective pericyte development. Fluorescence-activated cell sorting (FACS)-isolated myeloid cells and their progenitors from embryonic skin differentiate into pericytes in culture. At the molecular level, transforming growth factor-β (TGF-β) induces pericyte differentiation in culture. Furthermore, type 2 TGF-β receptor (Tgfbr2) mutants exhibit deficient pericyte development in skin vasculature. Combined, these data suggest that pericytes differentiate from tissue myeloid progenitors in the skin vasculature through TGF-β signaling.",
keywords = "TGF-β, brain, capillary blood vessel, fate mapping, mural cell, myeloid, pericyte, skin, tissue macrophage, vascular development",
author = "Tomoko Yamazaki and Ani Nalbandian and Yutaka Uchida and Wenling Li and Arnold, {Thomas D.} and Yoshiaki Kubota and Seiji Yamamoto and Masatsugu Ema and Mukouyama, {Yoh suke}",
note = "Funding Information: We thank W.B. Stallcup for providing anti-PDGFRβ and anti-NG2 antibodies, T. M{\"u}ller for providing anti-BFABP antibody, S. Suzu for providing M-CSF, H. Singh for providing PU.1 mutant mice, M. Herold for providing Vav-CreER mice, and R.W. Dettman for providing WT1-Cre driver mice. Thanks to L. Samsel, V. Dominical, P. Dagur, and P.J. McCoy for FACS assistance; J. Hawkins and the staff of NIH Bldg50 animal facility for assistance with mouse breeding and care; K. Gill for laboratory management and technical support; and R. Reed and F. Baldrey for administrative assistance. Thanks also to R.S. Adelstein, R. Izen, and I. Garcia-Pak for editorial advice on the manuscript; A.M. Michelson, R.S. Balaban, C. Iwata, and members of Laboratory of Stem Cell and Neuro-Vascular Biology for technical help and thoughtful discussion. T. Yamazaki was supported by the Japan Society for the Promotion of Science (JSPS) NIH-KAITOKU. This work was supported by the Intramural Research Program of the National Heart, Lung, and Blood Institute, NIH (HL005702-10 to Y.M.). Publisher Copyright: {\textcopyright} 2017",
year = "2017",
month = mar,
day = "21",
doi = "10.1016/j.celrep.2017.02.069",
language = "English",
volume = "18",
pages = "2991--3004",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "12",
}