Publication

Endothelial Plasticity: Shifting Phenotypes through Force Feedback

Krenning, G., Barauna, V. G., Krieger, J. E., Harmsen, M. C. & Moonen, J-R. A. J., 2016, In : Stem cells international. 2016, 15 p., 9762959.

Research output: Contribution to journalReview articleAcademicpeer-review

APA

Krenning, G., Barauna, V. G., Krieger, J. E., Harmsen, M. C., & Moonen, J-R. A. J. (2016). Endothelial Plasticity: Shifting Phenotypes through Force Feedback. Stem cells international, 2016, [9762959]. https://doi.org/10.1155/2016/9762959

Author

Krenning, Guido ; Barauna, Valerio G. ; Krieger, Jose E. ; Harmsen, Martin C. ; Moonen, Jan-Renier A. J. / Endothelial Plasticity : Shifting Phenotypes through Force Feedback. In: Stem cells international. 2016 ; Vol. 2016.

Harvard

Krenning, G, Barauna, VG, Krieger, JE, Harmsen, MC & Moonen, J-RAJ 2016, 'Endothelial Plasticity: Shifting Phenotypes through Force Feedback', Stem cells international, vol. 2016, 9762959. https://doi.org/10.1155/2016/9762959

Standard

Endothelial Plasticity : Shifting Phenotypes through Force Feedback. / Krenning, Guido; Barauna, Valerio G.; Krieger, Jose E.; Harmsen, Martin C.; Moonen, Jan-Renier A. J.

In: Stem cells international, Vol. 2016, 9762959, 2016.

Research output: Contribution to journalReview articleAcademicpeer-review

Vancouver

Krenning G, Barauna VG, Krieger JE, Harmsen MC, Moonen J-RAJ. Endothelial Plasticity: Shifting Phenotypes through Force Feedback. Stem cells international. 2016;2016. 9762959. https://doi.org/10.1155/2016/9762959


BibTeX

@article{6d177fb0be2c4965baed73ae79524588,
title = "Endothelial Plasticity: Shifting Phenotypes through Force Feedback",
abstract = "The endothelial lining of the vasculature is exposed to a large variety of biochemical and hemodynamic stimuli with different gradients throughout the vascular network. Adequate adaptation requires endothelial cells to be highly plastic, which is reflected by the remarkable heterogeneity of endothelial cells in tissues and organs. Hemodynamic forces such as fluid shear stress and cyclic strain are strong modulators of the endothelial phenotype and function. Although endothelial plasticity is essential during development and adult physiology, proatherogenic stimuli can induce adverse plasticity which contributes to disease. Endothelial-to-mesenchymal transition (EndMT), the hallmark of endothelial plasticity, was long thought to be restricted to embryonic development but has emerged as a pathologic process in a plethora of diseases. In this perspective we argue how shear stress and cyclic strain can modulate EndMT and discuss how this is reflected in atherosclerosis and pulmonary arterial hypertension.",
keywords = "FLUID SHEAR-STRESS, TO-MESENCHYMAL TRANSITION, GROWTH-FACTOR-BETA, PULMONARY ARTERIAL-HYPERTENSION, KRUPPEL-LIKE FACTOR-4, SMOOTH-MUSCLE-CELLS, ERK5 TRANSCRIPTIONAL ACTIVITY, GENE-EXPRESSION PROFILE, SAPHENOUS-VEIN GRAFTS, II TYPE-1 RECEPTOR",
author = "Guido Krenning and Barauna, {Valerio G.} and Krieger, {Jose E.} and Harmsen, {Martin C.} and Moonen, {Jan-Renier A. J.}",
year = "2016",
doi = "10.1155/2016/9762959",
language = "English",
volume = "2016",
journal = "Stem cells international",
issn = "1687-966X",
publisher = "HINDAWI LTD",

}

RIS

TY - JOUR

T1 - Endothelial Plasticity

T2 - Shifting Phenotypes through Force Feedback

AU - Krenning, Guido

AU - Barauna, Valerio G.

AU - Krieger, Jose E.

AU - Harmsen, Martin C.

AU - Moonen, Jan-Renier A. J.

PY - 2016

Y1 - 2016

N2 - The endothelial lining of the vasculature is exposed to a large variety of biochemical and hemodynamic stimuli with different gradients throughout the vascular network. Adequate adaptation requires endothelial cells to be highly plastic, which is reflected by the remarkable heterogeneity of endothelial cells in tissues and organs. Hemodynamic forces such as fluid shear stress and cyclic strain are strong modulators of the endothelial phenotype and function. Although endothelial plasticity is essential during development and adult physiology, proatherogenic stimuli can induce adverse plasticity which contributes to disease. Endothelial-to-mesenchymal transition (EndMT), the hallmark of endothelial plasticity, was long thought to be restricted to embryonic development but has emerged as a pathologic process in a plethora of diseases. In this perspective we argue how shear stress and cyclic strain can modulate EndMT and discuss how this is reflected in atherosclerosis and pulmonary arterial hypertension.

AB - The endothelial lining of the vasculature is exposed to a large variety of biochemical and hemodynamic stimuli with different gradients throughout the vascular network. Adequate adaptation requires endothelial cells to be highly plastic, which is reflected by the remarkable heterogeneity of endothelial cells in tissues and organs. Hemodynamic forces such as fluid shear stress and cyclic strain are strong modulators of the endothelial phenotype and function. Although endothelial plasticity is essential during development and adult physiology, proatherogenic stimuli can induce adverse plasticity which contributes to disease. Endothelial-to-mesenchymal transition (EndMT), the hallmark of endothelial plasticity, was long thought to be restricted to embryonic development but has emerged as a pathologic process in a plethora of diseases. In this perspective we argue how shear stress and cyclic strain can modulate EndMT and discuss how this is reflected in atherosclerosis and pulmonary arterial hypertension.

KW - FLUID SHEAR-STRESS

KW - TO-MESENCHYMAL TRANSITION

KW - GROWTH-FACTOR-BETA

KW - PULMONARY ARTERIAL-HYPERTENSION

KW - KRUPPEL-LIKE FACTOR-4

KW - SMOOTH-MUSCLE-CELLS

KW - ERK5 TRANSCRIPTIONAL ACTIVITY

KW - GENE-EXPRESSION PROFILE

KW - SAPHENOUS-VEIN GRAFTS

KW - II TYPE-1 RECEPTOR

U2 - 10.1155/2016/9762959

DO - 10.1155/2016/9762959

M3 - Review article

C2 - 26904133

VL - 2016

JO - Stem cells international

JF - Stem cells international

SN - 1687-966X

M1 - 9762959

ER -

ID: 29115070