Asset Details
Do you wish to reserve the book?
Vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic stress
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic stress
Do you wish to request the book?
Vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic stress
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic stress
2019
Overview
The intermediate filament (IF) cytoskeleton has been proposed to regulate morphogenic processes by integrating the cell fate signaling machinery with mechanical cues. Signaling between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) through the Notch pathway regulates arterial remodeling in response to changes in blood flow. Here we show that the IF-protein vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic forces. Vimentin is important for Notch transactivation by ECs and vimentin knockout mice (VimKO) display disrupted VSMC differentiation and adverse remodeling in aortic explants and
in vivo
. Shear stress increases Jagged1 levels and Notch activation in a vimentin-dependent manner. Shear stress induces phosphorylation of vimentin at serine 38 and phosphorylated vimentin interacts with Jagged1 and increases Notch activation potential. Reduced Jagged1-Notch transactivation strength disrupts lateral signal induction through the arterial wall leading to adverse remodeling. Taken together we demonstrate that vimentin forms a central part of a mechanochemical transduction pathway that regulates multilayer communication and structural homeostasis of the arterial wall.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/1
/ 13/106
/ 13/51
/ 14
/ 14/19
/ 14/63
/ 38
/ 38/77
/ 38/90
/ Animals
/ Aorta
/ Explants
/ Human Umbilical Vein Endothelial Cells
/ Humanities and Social Sciences
/ Humans
/ Jagged-1 Protein - metabolism
/ Mice
/ Muscle, Smooth, Vascular - metabolism
/ Myocytes, Smooth Muscle - metabolism
/ Receptors, Notch - metabolism
/ Science
/ Serine
/ Vimentin
