Repository logo
Log in(current)
Repository logoMIT Open ScholarshipDSpace@MIT
  1. Home
  2. MIT Open Access Articles
  3. MIT Open Access Articles
  4. Endothelium-derived fibronectin regulates neonatal vascular morphogenesis in an autocrine fashion

Endothelium-derived fibronectin regulates neonatal vascular morphogenesis in an autocrine fashion

Thumbnail Image
Download
Name

10456_2017_Article_9563.pdf

Size

8.89 MB

Format

Adobe PDF

Checksum (MD5)

e1f1f032942643e7a9b1924b7117acff

Download all files submitted through automated deposit
art_5370173129604114094.zip (8.51 MB)
Author(s)
Turner, Christopher
•
Hynes, Richard O.
•
Badu-Nkansah, Kwabena
Date Issued
June 2017
Journal
Angiogenesis
Publisher
Springer-Verlag
Citation
Turner, Christopher J.; Badu-Nkansah, Kwabena and Hynes, Richard O. “Endothelium-Derived Fibronectin Regulates Neonatal Vascular Morphogenesis in an Autocrine Fashion.” Angiogenesis 20, 1 (June 2017): 1-13 © 2017 The Author(s)
Version
Final published version
Abstract
Fibronectin containing alternatively spliced EIIIA and EIIIB domains is largely absent from mature quiescent vessels in adults, but is highly expressed around blood vessels during developmental and pathological angiogenesis. The precise functions of fibronectin and its splice variants during developmental angiogenesis however remain unclear due to the presence of cardiac, somitic, mesodermal and neural defects in existing global fibronectin KO mouse models. Using a rare family of surviving EIIIA EIIIB double KO mice, as well as inducible endothelial-specific fibronectin-deficient mutant mice, we show that vascular development in the neonatal retina is regulated in an autocrine manner by endothelium-derived fibronectin, and requires both EIIIA and EIIIB domains and the RGD-binding α5 and αv integrins for its function. Exogenous sources of fibronectin do not fully substitute for the autocrine function of endothelial fibronectin, demonstrating that fibronectins from different sources contribute differentially to specific aspects of angiogenesis.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution
http://creativecommons.org/licenses/by/4.0/
Persistent DSpace Link
http://hdl.handle.net/1721.1/110606
DOI of Published Version
https://doi.org/10.1007/s10456-017-9563-8
Repository logo
PrivacyPermissionsAccessibilityContact us
Repository logo
Notify us about copyright concerns.