10.5061/DRYAD.B8D0G
Andersen, Nicholas J.
Frederik Meijer Heart and Vascular Institute, Spectrum Hospital, 100
Michigan St. NE, Grand Rapids, MI, 49503, United States of America
Boguslawski, Elissa A.
Laboratory of Cancer and Developmental Cell Biology, Center for Cancer
Cell Biology, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand
Rapids, MI, 49503, United States of America
Naidu, Agni S.
Laboratory of Cancer and Developmental Cell Biology, Center for Cancer
Cell Biology, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand
Rapids, MI, 49503, United States of America
Szot, Christopher
National Cancer Institute
Bromberg-White, Jennifer L.
Laboratory of Cancer and Developmental Cell Biology, Center for Cancer
Cell Biology, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand
Rapids, MI, 49503, United States of America
Kits, Kara
Laboratory of Cancer and Developmental Cell Biology, Center for Cancer
Cell Biology, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand
Rapids, MI, 49503, United States of America
Kuk, Cynthia Y.
Laboratory of Cancer and Developmental Cell Biology, Center for Cancer
Cell Biology, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand
Rapids, MI, 49503, United States of America
Holton, Laura E.
Frederik Meijer Heart and Vascular Institute, Spectrum Hospital, 100
Michigan St. NE, Grand Rapids, MI, 49503, United States of America
St. Croix, Bradley
National Cancer Institute
Chambers, Christopher M.
Duesbery, Nicholas S.
Laboratory of Cancer and Developmental Cell Biology, Center for Cancer
Cell Biology, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand
Rapids, MI, 49503, United States of America
Data from: Anthrax toxin receptor 1 is essential for arteriogenesis in a
mouse model of hindlimb ischemia
Dryad
dataset
2016
2016-11-25T00:00:00Z
2016-11-25T00:00:00Z
en
https://doi.org/10.1371/journal.pone.0146586
104301 bytes
1
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Anthrax toxin receptor 1/tumor endothelial marker 8 (Antxr1 or TEM8) is
up-regulated in tumor vasculature and serves as a receptor for anthrax
toxin, but its physiologic function is unclear. The objective of this
study was to evaluate the role of Antxr1 in arteriogenesis. The role of
Antxr1 in arteriogenesis was tested by measuring gene expression and
immunohistochemistry in a mouse model of hindlimb ischemia using wild-type
and ANTXR1-/- mice. Additional tests were performed by measuring gene
expression in in vitro models of fluid shear stress and hypoxia, as well
as in human muscle tissues obtained from patients having peripheral artery
disease. We observed that Antxr1 expression transiently increased in
ischemic tissues following femoral artery ligation and that its expression
was necessary for arteriogenesis. In the absence of Antxr1, the mean
arterial lumen area in ischemic tissues decreased. Antxr1 mRNA and protein
expression was positively regulated by fluid shear stress, but not by
hypoxia. Furthermore, Antxr1 expression was elevated in human peripheral
artery disease requiring lower extremity bypass surgery. These findings
demonstrate an essential physiologic role for Antxr1 in arteriogenesis and
peripheral artery disease, with important implications for managing
ischemia and other arteriogenesis-dependent vascular diseases.
Andersen PLoS One 2015This file contains data used to generate the figures
in this manuscript.