Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells

Arkady Rutkovskiy, Maria Lund, Tanja Saman Siamansour, Trine Marita Reine, Svein Olav Kolset, Kristin Larsen Sand, Elena Ignatieva, Mikhail L. Gordeev, Kare Olav Stensløkken, Guro Valen, Jarle Vaage, Anna Malashicheva

Результат исследований: Научные публикации в периодических изданияхстатья

2 Цитирования (Scopus)

Выдержка

Objectives: Vascular wall calcification is a major pathophysiological component of atherosclerotic disease with many similarities to osteogenesis. Mechanical stress of the vascular wall may theoretically contribute to the proliferative processes by endothelial and interstitial cells. The aim of the study was to investigate the effect of mechanical stress on the expression of some calcification-related genes in primary human endothelial and interstitial cells, and how endothelial cells may stimulate the fibroblast and smooth muscle cells. Methods: Human umbilical vein endothelial and interstitial cells were subjected to cyclic stretch using a FlexCell® bioreactor, and interstitial cells were also subjected to tensile strain in cultures embedded in 3-dimensional collagen gels. The medium from endothelial cells was used to stimulate the gel-cultured interstitial cells, or the endothelium was sown directly on top. For comparison, human endothelial and smooth muscle cells were isolated from aortic wall fragments of patients with and without the aortic aneurysm. The expression of genes was measured using quantitative PCR. Results: Four hours of cyclic stretch applied to cultured endothelial cells upregulated the mRNA expression of bone morphogenetic protein 2 (BMP-2), a major procalcific growth factor. When applied to a 3-dimensional culture of vascular interstitial cells, the medium from prestretched endothelial cells decreased the expression of BMP-2 and periostin mRNA in the fibroblasts. The static tension in gel-cultured interstitial cells upregulated BMP-2 mRNA expression. The addition of endothelial cells on the top of this culture also reduced mRNA of anticalcific genes, periostin and osteopontin. Similar changes were observed in smooth muscle cells from human aortic aneurysms compared to cells from the healthy aorta. Aortic aneurysm endothelial cells also showed an increased expression of BMP-2 mRNA. Conclusions: Endothelial cells respond to mechanical stress by upregulation of pro-osteogenic factor BMP-2 mRNA and modulate the expression of other osteogenic factors in vascular interstitial cells. Endothelial cells may, thus, contribute to vascular calcification when exposed to mechanical stress.

Язык оригиналаанглийский
Страницы (с-по)803-811
Число страниц9
ЖурналInteractive Cardiovascular and Thoracic Surgery
Том28
Номер выпуска5
DOI
СостояниеОпубликовано - 1 янв 2019

Отпечаток

Mechanical Stress
Endothelial Cells
Bone Morphogenetic Protein 2
Genes
Messenger RNA
Aortic Aneurysm
Smooth Muscle Myocytes
Vascular Calcification
Cultured Cells
Gels
Blood Vessels
Fibroblasts
Osteopontin
Human Umbilical Vein Endothelial Cells
Bioreactors
Osteogenesis
Endothelium
Aorta
Intercellular Signaling Peptides and Proteins
Up-Regulation

Предметные области Scopus

  • Хирургия
  • Пульмонология и респираторная медицина
  • Кардиология и сердечно-сосудистая медицина

Цитировать

Rutkovskiy, Arkady ; Lund, Maria ; Siamansour, Tanja Saman ; Reine, Trine Marita ; Kolset, Svein Olav ; Sand, Kristin Larsen ; Ignatieva, Elena ; Gordeev, Mikhail L. ; Stensløkken, Kare Olav ; Valen, Guro ; Vaage, Jarle ; Malashicheva, Anna. / Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells. В: Interactive Cardiovascular and Thoracic Surgery. 2019 ; Том 28, № 5. стр. 803-811.
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abstract = "Objectives: Vascular wall calcification is a major pathophysiological component of atherosclerotic disease with many similarities to osteogenesis. Mechanical stress of the vascular wall may theoretically contribute to the proliferative processes by endothelial and interstitial cells. The aim of the study was to investigate the effect of mechanical stress on the expression of some calcification-related genes in primary human endothelial and interstitial cells, and how endothelial cells may stimulate the fibroblast and smooth muscle cells. Methods: Human umbilical vein endothelial and interstitial cells were subjected to cyclic stretch using a FlexCell{\circledR} bioreactor, and interstitial cells were also subjected to tensile strain in cultures embedded in 3-dimensional collagen gels. The medium from endothelial cells was used to stimulate the gel-cultured interstitial cells, or the endothelium was sown directly on top. For comparison, human endothelial and smooth muscle cells were isolated from aortic wall fragments of patients with and without the aortic aneurysm. The expression of genes was measured using quantitative PCR. Results: Four hours of cyclic stretch applied to cultured endothelial cells upregulated the mRNA expression of bone morphogenetic protein 2 (BMP-2), a major procalcific growth factor. When applied to a 3-dimensional culture of vascular interstitial cells, the medium from prestretched endothelial cells decreased the expression of BMP-2 and periostin mRNA in the fibroblasts. The static tension in gel-cultured interstitial cells upregulated BMP-2 mRNA expression. The addition of endothelial cells on the top of this culture also reduced mRNA of anticalcific genes, periostin and osteopontin. Similar changes were observed in smooth muscle cells from human aortic aneurysms compared to cells from the healthy aorta. Aortic aneurysm endothelial cells also showed an increased expression of BMP-2 mRNA. Conclusions: Endothelial cells respond to mechanical stress by upregulation of pro-osteogenic factor BMP-2 mRNA and modulate the expression of other osteogenic factors in vascular interstitial cells. Endothelial cells may, thus, contribute to vascular calcification when exposed to mechanical stress.",
keywords = "Aortic aneurysm, Cocultures, Ectopic calcification, Endothelial cells, Mechanical stress",
author = "Arkady Rutkovskiy and Maria Lund and Siamansour, {Tanja Saman} and Reine, {Trine Marita} and Kolset, {Svein Olav} and Sand, {Kristin Larsen} and Elena Ignatieva and Gordeev, {Mikhail L.} and Stensl{\o}kken, {Kare Olav} and Guro Valen and Jarle Vaage and Anna Malashicheva",
year = "2019",
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doi = "10.1093/icvts/ivy339",
language = "English",
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journal = "Interactive Cardiovascular and Thoracic Surgery",
issn = "1569-9293",
publisher = "European Association for Cardio-Thoracic Surgery",
number = "5",

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Rutkovskiy, A, Lund, M, Siamansour, TS, Reine, TM, Kolset, SO, Sand, KL, Ignatieva, E, Gordeev, ML, Stensløkken, KO, Valen, G, Vaage, J & Malashicheva, A 2019, 'Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells', Interactive Cardiovascular and Thoracic Surgery, том. 28, № 5, стр. 803-811. https://doi.org/10.1093/icvts/ivy339

Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells. / Rutkovskiy, Arkady; Lund, Maria; Siamansour, Tanja Saman; Reine, Trine Marita; Kolset, Svein Olav; Sand, Kristin Larsen; Ignatieva, Elena; Gordeev, Mikhail L.; Stensløkken, Kare Olav; Valen, Guro; Vaage, Jarle; Malashicheva, Anna.

В: Interactive Cardiovascular and Thoracic Surgery, Том 28, № 5, 01.01.2019, стр. 803-811.

Результат исследований: Научные публикации в периодических изданияхстатья

TY - JOUR

T1 - Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells

AU - Rutkovskiy, Arkady

AU - Lund, Maria

AU - Siamansour, Tanja Saman

AU - Reine, Trine Marita

AU - Kolset, Svein Olav

AU - Sand, Kristin Larsen

AU - Ignatieva, Elena

AU - Gordeev, Mikhail L.

AU - Stensløkken, Kare Olav

AU - Valen, Guro

AU - Vaage, Jarle

AU - Malashicheva, Anna

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Objectives: Vascular wall calcification is a major pathophysiological component of atherosclerotic disease with many similarities to osteogenesis. Mechanical stress of the vascular wall may theoretically contribute to the proliferative processes by endothelial and interstitial cells. The aim of the study was to investigate the effect of mechanical stress on the expression of some calcification-related genes in primary human endothelial and interstitial cells, and how endothelial cells may stimulate the fibroblast and smooth muscle cells. Methods: Human umbilical vein endothelial and interstitial cells were subjected to cyclic stretch using a FlexCell® bioreactor, and interstitial cells were also subjected to tensile strain in cultures embedded in 3-dimensional collagen gels. The medium from endothelial cells was used to stimulate the gel-cultured interstitial cells, or the endothelium was sown directly on top. For comparison, human endothelial and smooth muscle cells were isolated from aortic wall fragments of patients with and without the aortic aneurysm. The expression of genes was measured using quantitative PCR. Results: Four hours of cyclic stretch applied to cultured endothelial cells upregulated the mRNA expression of bone morphogenetic protein 2 (BMP-2), a major procalcific growth factor. When applied to a 3-dimensional culture of vascular interstitial cells, the medium from prestretched endothelial cells decreased the expression of BMP-2 and periostin mRNA in the fibroblasts. The static tension in gel-cultured interstitial cells upregulated BMP-2 mRNA expression. The addition of endothelial cells on the top of this culture also reduced mRNA of anticalcific genes, periostin and osteopontin. Similar changes were observed in smooth muscle cells from human aortic aneurysms compared to cells from the healthy aorta. Aortic aneurysm endothelial cells also showed an increased expression of BMP-2 mRNA. Conclusions: Endothelial cells respond to mechanical stress by upregulation of pro-osteogenic factor BMP-2 mRNA and modulate the expression of other osteogenic factors in vascular interstitial cells. Endothelial cells may, thus, contribute to vascular calcification when exposed to mechanical stress.

AB - Objectives: Vascular wall calcification is a major pathophysiological component of atherosclerotic disease with many similarities to osteogenesis. Mechanical stress of the vascular wall may theoretically contribute to the proliferative processes by endothelial and interstitial cells. The aim of the study was to investigate the effect of mechanical stress on the expression of some calcification-related genes in primary human endothelial and interstitial cells, and how endothelial cells may stimulate the fibroblast and smooth muscle cells. Methods: Human umbilical vein endothelial and interstitial cells were subjected to cyclic stretch using a FlexCell® bioreactor, and interstitial cells were also subjected to tensile strain in cultures embedded in 3-dimensional collagen gels. The medium from endothelial cells was used to stimulate the gel-cultured interstitial cells, or the endothelium was sown directly on top. For comparison, human endothelial and smooth muscle cells were isolated from aortic wall fragments of patients with and without the aortic aneurysm. The expression of genes was measured using quantitative PCR. Results: Four hours of cyclic stretch applied to cultured endothelial cells upregulated the mRNA expression of bone morphogenetic protein 2 (BMP-2), a major procalcific growth factor. When applied to a 3-dimensional culture of vascular interstitial cells, the medium from prestretched endothelial cells decreased the expression of BMP-2 and periostin mRNA in the fibroblasts. The static tension in gel-cultured interstitial cells upregulated BMP-2 mRNA expression. The addition of endothelial cells on the top of this culture also reduced mRNA of anticalcific genes, periostin and osteopontin. Similar changes were observed in smooth muscle cells from human aortic aneurysms compared to cells from the healthy aorta. Aortic aneurysm endothelial cells also showed an increased expression of BMP-2 mRNA. Conclusions: Endothelial cells respond to mechanical stress by upregulation of pro-osteogenic factor BMP-2 mRNA and modulate the expression of other osteogenic factors in vascular interstitial cells. Endothelial cells may, thus, contribute to vascular calcification when exposed to mechanical stress.

KW - Aortic aneurysm

KW - Cocultures

KW - Ectopic calcification

KW - Endothelial cells

KW - Mechanical stress

UR - http://www.scopus.com/inward/record.url?scp=85064904716&partnerID=8YFLogxK

U2 - 10.1093/icvts/ivy339

DO - 10.1093/icvts/ivy339

M3 - Article

AN - SCOPUS:85064904716

VL - 28

SP - 803

EP - 811

JO - Interactive Cardiovascular and Thoracic Surgery

JF - Interactive Cardiovascular and Thoracic Surgery

SN - 1569-9293

IS - 5

ER -