Malashicheva Anna, Kostina Daria, Kostina Aleksandra, Irtyuga Olga, Voronkina Irina, Smagina Larisa, Ignatieva Elena, Gavriliuk Natalia, Uspensky Vladimir, Moiseeva Olga, Vaage Jarle, Kostareva Anna
Almazov Federal Medical Research Centre, Akkuratova 2, Saint Petersburg 197341, Russia; Saint Petersburg State University, Universitetskaya Nab. 7/9, Saint Petersburg 199034, Russia; ITMO University, Institute of Translational Medicine, 49 Kronverksky Prospekt, Saint Petersburg 197101, Russia.
Almazov Federal Medical Research Centre, Akkuratova 2, Saint Petersburg 197341, Russia.
Int J Vasc Med. 2016;2016:3107879. doi: 10.1155/2016/3107879. Epub 2016 Jan 19.
Thoracic aortic aneurysm develops as a result of complex series of events that alter the cellular structure and the composition of the extracellular matrix of the aortic wall. The purpose of the present work was to study the cellular functions of endothelial and smooth muscle cells from the patients with aneurysms of the thoracic aorta. We studied endothelial and smooth muscle cells from aneurysms in patients with bicuspid aortic valve and with tricuspid aortic valve. The expression of key markers of endothelial (CD31, vWF, and VE-cadherin) and smooth muscle (SMA, SM22α, calponin, and vimentin) cells as well extracellular matrix and MMP activity was studied as well as and apoptosis and cell proliferation. Expression of functional markers of endothelial and smooth muscle cells was reduced in patient cells. Cellular proliferation, migration, and synthesis of extracellular matrix proteins are attenuated in the cells of the patients. We show for the first time that aortic endothelial cell phenotype is changed in the thoracic aortic aneurysms compared to normal aortic wall. In conclusion both endothelial and smooth muscle cells from aneurysms of the ascending aorta have downregulated specific cellular markers and altered functional properties, such as growth rate, apoptosis induction, and extracellular matrix synthesis.
胸主动脉瘤是由一系列复杂事件导致的，这些事件改变了主动脉壁的细胞结构和细胞外基质的组成。本研究的目的是探讨胸主动脉瘤患者内皮细胞和平滑肌细胞的细胞功能。我们研究了二叶式主动脉瓣和三叶式主动脉瓣患者动脉瘤的内皮细胞和平滑肌细胞。研究了内皮细胞（CD31、vWF和VE-钙黏蛋白）和平滑肌细胞（SMA、SM22α、钙调蛋白和波形蛋白）的关键标志物表达，以及细胞外基质和MMP活性，同时研究了细胞凋亡和细胞增殖情况。患者细胞中内皮细胞和平滑肌细胞功能标志物的表达降低。患者细胞中的细胞增殖、迁移和细胞外基质蛋白合成减弱。我们首次表明，与正常主动脉壁相比，胸主动脉瘤中主动脉内皮细胞表型发生了改变。总之，升主动脉瘤的内皮细胞和平滑肌细胞均下调了特定的细胞标志物，并改变了功能特性，如生长速率、凋亡诱导和细胞外基质合成。
