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(searched for: Functional-Roles-of-Shear-Stress-in-Vascular-Endothelial-Cells)
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Lowell T. Edgar, Sciprofile linkClaudio A. Franco, Holger Gerhardt, Miguel Oscar Bernabeu
Published: 7 February 2020
The publisher has not yet granted permission to display this abstract.
Vedanta Mehta, Kar-Lai Pang, Daniel Rozbesky, Katrin Nather, Adam Keen, Dariusz Lachowski, Youxin Kong, Dimple Karia, Michael Ameismeier, Jianhua Huang, et al.
Published: 5 February 2020
Nature, Volume 578, pp 290-295; doi:10.1038/s41586-020-1979-4

The publisher has not yet granted permission to display this abstract.
Yangzi Isabel Tian, Xulang Zhang, Karen Torrejon, John Danias, Sofya Gindina, Ashima Nayyar, Sciprofile linkYiqin Du, Sciprofile linkYubing Xie
Published: 23 January 2020
Acta Biomaterialia; doi:10.1016/j.actbio.2020.01.033

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Qingsong Hu, Tao Zhang, Yan Li, Jianyi Feng, RuQiong Nie, Xiaoqing Wang, Changnong Peng, Xiao Ke
Journal of Hypertension, Volume 38, pp 82-94; doi:10.1097/hjh.0000000000002203

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‡ Soo Mi Ki1, ‡ Ji Hyun Kim1, ‡ So Yeon Won1, Shin Ji Oh1,
In
Young Lee2, Young‐Ki Bae3, Ki Wha Chung4, Byung‐Ok Choi5, Boyoun Park6, Eui‐Ju Choi, et al.
Published: 29 December 2019
by EMBO
EMBO reports, Volume 21; doi:10.15252/embr.201948290

Abstract: The
endothelial
cilium is a microtubule-based organelle responsible for blood flow-induced mechanosensation and signal transduction during angiogenesis. The precise
function
and mechanisms by which ciliary mechanosensation occurs, however, are poorly understood. Although posttranslational modifications (PTMs)
of
cytoplasmic tubulin are known to be important
in
angiogenesis, the specific
roles
of
ciliary tubulin PTMs play remain unclear. Here, we report that loss
of
centrosomal protein 41 (CEP41) results
in
vascular
impairment
in
human
cell
lines and zebrafish, implying a previously unknown pro-angiogenic
role
for CEP41. We show that proper control
of
tubulin glutamylation by CEP41 is necessary for cilia disassembly and that is involved
in
endothelial
cell
(EC) dynamics such as migration and tubulogenesis. We show that
in
ECs responding to
shear
stress
or hypoxia, CEP41 activates Aurora kinase A (AURKA) and upregulates expression
of
VEGFA and VEGFR2 through ciliary tubulin glutamylation, as well as leads to the deciliation. We further show that
in
hypoxia-induced angiogenesis, CEP41 is responsible for the activation
of
HIF1α to trigger the AURKA-VEGF pathway. Overall, our results suggest the CEP41-HIF1α-AURKA-VEGF axis as a key molecular mechanism
of
angiogenesis and demonstrate how important ciliary tubulin glutamylation is
in
mechanosense-responded EC dynamics.
Emmanouil Korakas, Sciprofile linkIgnatios Ikonomidis, Konstantinos Markakis, Athanasios Raptis, George Dimitriadis, Sciprofile linkVaia Lambadiari
Current Vascular Pharmacology, Volume 18, pp 1-1; doi:10.2174/1570161118666191224120242

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Gangqi Wang, Sarantos Kostidis, Gesa L. Tiemeier, Wendy M.P.J. Sol, Margreet R. De Vries, Martin Giera, Peter Carmeliet, Bernard M. Van Den Berg, Ton J. Rabelink
Arteriosclerosis, Thrombosis, and Vascular Biology, Volume 40, pp 350-364; doi:10.1161/ATVBAHA.119.313399

The publisher has not yet granted permission to display this abstract.
Jihwa Chung, Kyoung Hwa Kim, Shung Hyun An, Sunmi Lee, Byung-Kwan Lim, Sang Won Kang, Sciprofile linkKihwan Kwon
Experimental & Molecular Medicine, Volume 51, pp 144-15; doi:10.1038/s12276-019-0347-7

Abstract:
Endothelial
mechanotransduction by fluid
shear
stress
(FSS) modulates
endothelial
function
and
vascular
pathophysiology through mechanosensors on the
cell
membrane. The coxsackievirus and adenovirus receptor (CAR) is not only a viral receptor but also a component
of
tight junctions and plays an important
role
in
tissue homeostasis. Here, we demonstrate the expression, regulatory mechanism, and
role
of
CAR
in
vascular
endothelial
cells
(ECs) under FSS conditions. Disturbed flow increased, whereas unidirectional laminar
shear
stress
(LSS) decreased, CAR expression
in
ECs through the Krüppel-like factor 2 (KLF2)/activator protein 1 (AP-1) axis. Deletion
of
CAR reduced the expression
of
proinflammatory genes and
endothelial
inflammation induced by disturbed flow via the suppression
of
NF-κB activation. Consistently, disturbed flow-induced atherosclerosis was reduced
in
EC-specific CAR KO mice. CAR was found to be involved
in
endothelial
mechanotransduction through the regulation
of
platelet
endothelial
cell
adhesion molecule 1 (PECAM-1) phosphorylation. Our results demonstrate that
endothelial
CAR is regulated by FSS and that this regulated CAR acts as an important modulator
of
endothelial
mechanotransduction by FSS.
Abdullah Kutlar, Jennifer Pollock, Steffen E. Meiler, Ryan Harris, Xu HongYan, Leigh Wells, Latanya Bowman, Sharon Jones, David M. Pollock
Published: 13 November 2019
Blood, Volume 134, pp 617-617; doi:10.1182/blood-2019-130036

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Yongzhi Qiu, Yumiko Sakurai, Wilbur A. Lam
Published: 13 November 2019
Blood, Volume 134, pp 441-441; doi:10.1182/blood-2019-128718

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