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Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve. / Kostina, Aleksandra S.; Uspensky, Vladimir E.; Irtyuga, Olga B.; Ignatieva, Elena V.; Freylikhman, Olga; Gavriliuk, Natalia D.; Moiseeva, Olga M.; Zhuk, Sergey; Tomilin, Alexey; Kostareva, Anna A.; Malashicheva, Anna B.

In: Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1862, No. 4, 04.2016, p. 733-740.

Research output: Contribution to journalArticlepeer-review

Harvard

Kostina, AS, Uspensky, VE, Irtyuga, OB, Ignatieva, EV, Freylikhman, O, Gavriliuk, ND, Moiseeva, OM, Zhuk, S, Tomilin, A, Kostareva, AA & Malashicheva, AB 2016, 'Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve', Biochimica et Biophysica Acta - Molecular Basis of Disease, vol. 1862, no. 4, pp. 733-740. https://doi.org/10.1016/j.bbadis.2016.02.006, https://doi.org/10.1016/j.bbadis.2016.02.006

APA

Kostina, A. S., Uspensky, V. E., Irtyuga, O. B., Ignatieva, E. V., Freylikhman, O., Gavriliuk, N. D., Moiseeva, O. M., Zhuk, S., Tomilin, A., Kostareva, A. A., & Malashicheva, A. B. (2016). Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1862(4), 733-740. https://doi.org/10.1016/j.bbadis.2016.02.006, https://doi.org/10.1016/j.bbadis.2016.02.006

Vancouver

Kostina AS, Uspensky VE, Irtyuga OB, Ignatieva EV, Freylikhman O, Gavriliuk ND et al. Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve. Biochimica et Biophysica Acta - Molecular Basis of Disease. 2016 Apr;1862(4):733-740. https://doi.org/10.1016/j.bbadis.2016.02.006, https://doi.org/10.1016/j.bbadis.2016.02.006

Author

Kostina, Aleksandra S. ; Uspensky, Vladimir E. ; Irtyuga, Olga B. ; Ignatieva, Elena V. ; Freylikhman, Olga ; Gavriliuk, Natalia D. ; Moiseeva, Olga M. ; Zhuk, Sergey ; Tomilin, Alexey ; Kostareva, Anna A. ; Malashicheva, Anna B. / Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve. In: Biochimica et Biophysica Acta - Molecular Basis of Disease. 2016 ; Vol. 1862, No. 4. pp. 733-740.

BibTeX

@article{439110b503cc4dfc9ecbfb2d41b8c31b,
title = "Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve",
abstract = "Bicuspid aortic valve is the most common congenital heart malformation and the reasons for the aortopathies associated with bicuspid aortic valve remain unclear. NOTCH1 mutations are associated with bicuspid aortic valve and have been found in individuals with various left ventricular outflow tract abnormalities. Notch is a key signaling during cardiac valve formation that promotes the endothelial-to-mesenchymal transition. We address the role of Notch signaling in human aortic endothelial cells from patients with bicuspid aortic valve and aortic aneurysm. Aortic endothelial cells were isolated from tissue fragments of bicuspid aortic valve associated thoracic aortic aneurysm patients and from healthy donors. Endothelial-to-mesenchymal transition was induced by activation of Notch signaling. Effectiveness of the transition was estimated by loss of endothelial and gain of mesenchymal markers by immunocytochemistry and qPCR. We show that aortic endothelial cells from the patients with aortic aneurysm and bicuspid aortic valve have down regulated Notch signaling and fail to activate Notch-dependent endothelial-to-mesenchymal transition in response to its stimulation by different Notch ligands. Our findings support the idea that bicuspid aortic valve and associated aortic aneurysm is associated with dysregulation of the entire Notch signaling pathway independently on the specific gene mutation. (C) 2016 Elsevier B.V. All rights reserved.",
keywords = "Aorta, Endothelium, Valves, Signal transduction, MESENCHYMAL TRANSITION, DISEASE, MUTATIONS, GENE, ACTIVATION, MALFORMATIONS, MECHANISMS, DISORDERS, VEGF",
author = "Kostina, {Aleksandra S.} and Uspensky, {Vladimir E.} and Irtyuga, {Olga B.} and Ignatieva, {Elena V.} and Olga Freylikhman and Gavriliuk, {Natalia D.} and Moiseeva, {Olga M.} and Sergey Zhuk and Alexey Tomilin and Kostareva, {Anna A.} and Malashicheva, {Anna B.}",
year = "2016",
month = apr,
doi = "10.1016/j.bbadis.2016.02.006",
language = "Английский",
volume = "1862",
pages = "733--740",
journal = "Biochimica et Biophysica Acta - Molecular Basis of Disease",
issn = "0925-4439",
publisher = "Elsevier",
number = "4",

}

RIS

TY - JOUR

T1 - Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve

AU - Kostina, Aleksandra S.

AU - Uspensky, Vladimir E.

AU - Irtyuga, Olga B.

AU - Ignatieva, Elena V.

AU - Freylikhman, Olga

AU - Gavriliuk, Natalia D.

AU - Moiseeva, Olga M.

AU - Zhuk, Sergey

AU - Tomilin, Alexey

AU - Kostareva, Anna A.

AU - Malashicheva, Anna B.

PY - 2016/4

Y1 - 2016/4

N2 - Bicuspid aortic valve is the most common congenital heart malformation and the reasons for the aortopathies associated with bicuspid aortic valve remain unclear. NOTCH1 mutations are associated with bicuspid aortic valve and have been found in individuals with various left ventricular outflow tract abnormalities. Notch is a key signaling during cardiac valve formation that promotes the endothelial-to-mesenchymal transition. We address the role of Notch signaling in human aortic endothelial cells from patients with bicuspid aortic valve and aortic aneurysm. Aortic endothelial cells were isolated from tissue fragments of bicuspid aortic valve associated thoracic aortic aneurysm patients and from healthy donors. Endothelial-to-mesenchymal transition was induced by activation of Notch signaling. Effectiveness of the transition was estimated by loss of endothelial and gain of mesenchymal markers by immunocytochemistry and qPCR. We show that aortic endothelial cells from the patients with aortic aneurysm and bicuspid aortic valve have down regulated Notch signaling and fail to activate Notch-dependent endothelial-to-mesenchymal transition in response to its stimulation by different Notch ligands. Our findings support the idea that bicuspid aortic valve and associated aortic aneurysm is associated with dysregulation of the entire Notch signaling pathway independently on the specific gene mutation. (C) 2016 Elsevier B.V. All rights reserved.

AB - Bicuspid aortic valve is the most common congenital heart malformation and the reasons for the aortopathies associated with bicuspid aortic valve remain unclear. NOTCH1 mutations are associated with bicuspid aortic valve and have been found in individuals with various left ventricular outflow tract abnormalities. Notch is a key signaling during cardiac valve formation that promotes the endothelial-to-mesenchymal transition. We address the role of Notch signaling in human aortic endothelial cells from patients with bicuspid aortic valve and aortic aneurysm. Aortic endothelial cells were isolated from tissue fragments of bicuspid aortic valve associated thoracic aortic aneurysm patients and from healthy donors. Endothelial-to-mesenchymal transition was induced by activation of Notch signaling. Effectiveness of the transition was estimated by loss of endothelial and gain of mesenchymal markers by immunocytochemistry and qPCR. We show that aortic endothelial cells from the patients with aortic aneurysm and bicuspid aortic valve have down regulated Notch signaling and fail to activate Notch-dependent endothelial-to-mesenchymal transition in response to its stimulation by different Notch ligands. Our findings support the idea that bicuspid aortic valve and associated aortic aneurysm is associated with dysregulation of the entire Notch signaling pathway independently on the specific gene mutation. (C) 2016 Elsevier B.V. All rights reserved.

KW - Aorta

KW - Endothelium

KW - Valves

KW - Signal transduction

KW - MESENCHYMAL TRANSITION

KW - DISEASE

KW - MUTATIONS

KW - GENE

KW - ACTIVATION

KW - MALFORMATIONS

KW - MECHANISMS

KW - DISORDERS

KW - VEGF

U2 - 10.1016/j.bbadis.2016.02.006

DO - 10.1016/j.bbadis.2016.02.006

M3 - статья

VL - 1862

SP - 733

EP - 740

JO - Biochimica et Biophysica Acta - Molecular Basis of Disease

JF - Biochimica et Biophysica Acta - Molecular Basis of Disease

SN - 0925-4439

IS - 4

ER -

ID: 7567534