Atherosclerosis-prone branch regions in human aorta: microarchitecture and cell composition of intima

Kolpakov, Valeri; Polishchuk, Roman; Bannykh, Sergei I.; Rekhter, Mark D.; Solovjev, Pavel; Romanov, Yu. A.; Tararak, E.; Antonov, Alexander S.; Mirоnоv, Alexander A.

doi:10.1016/0021-9150(95)05735-8

Cited by 32 publications

(29 citation statements)

References 47 publications

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“…In these regions, the endothelial cell shape is round (31,32), the density of F-actin filaments is lower than those in other regions (33), and monocyte adhesion and migration were frequently observed (34). The increased shear stress in the contralateral common carotid artery to the ligated common carotid artery increases the elongation of the endothelial cells and F-actin filaments and decreases monocyte adhesion and migration (35).…”

Section: Discussionmentioning

confidence: 98%

Measurements of endothelial cell-to-cell and cell-to-substrate gaps and micromechanical properties of endothelial cells during monocyte adhesion

Kataoka

Iwaki

Hashimoto

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

119

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The interaction between monocytes and endothelial cells is considered to play a major role in the early stage of atherosclerosis, and the involved endothelial cell micromechanics may provide us with important aspects of atherogenesis. In the present study, we evaluated (i) the endothelial cell-to-cell and cell-to-substrate gaps with the electric cell-substrate impedance sensing system, which can detect the nanometer order changes of cell-to-cell and cell-tosubstrate distances separately, and (ii) the endothelial cell micromechanical properties with an atomic force microscope after application of monocytes to endothelial cells. Application of monocytic THP-1 cells to IL-1␤-stimulated human umbilical vein endothelial cells immediately decreased the electrical resistance of the endothelial cell-to-substrate (increase of the cell-to-substrate gap), whereas the endothelial cell-to-cell resistance (cell-to-cell gap) did not change. The elastic modulus of the endothelial cells decreased after 2-h monocyte application, indicating an increase of endothelial cell deformability. In conclusion, the interaction of the monocytes to the endothelial cells reduced the adhesiveness to the substrate and increased the deformability of endothelial cells. These changes in the adhesiveness and the deformability may facilitate migration of monocytes, a key process of atherogenesis in the later stage.A t the early stage of atherosclerosis, an aggregation of lipid-rich macrophages that were derived from monocytes was observed in the intima (1). Adhesion of monocytes to the arterial endothelial cells and their migration into the arterial intima are the earliest key events in atherogenesis (1). Previous studies demonstrated that leukocytes could migrate throughout the endothelial monolayer via not only paracellular but also transcellular pathways in vivo and in vitro (2-5). The endothelial cell micromechanics that are involved in endothelial cell micromotion and the mechanical properties of endothelial cells may be key factors in these processes. Earlier studies reported the importance of adhesion molecules in the adhesion and migration of monocytes to endothelial cells (6, 7). We previously demonstrated that the adhesion of monocytes to human umbilical vein endothelial cells (HUVEC) induces the decrease in the amount of focal adhesion kinase (p125 FAK ) with reduction of the density of F-actin stress fibers in HUVEC (8). These results suggest that the adhesion of monocytes induces changes of the adhesiveness of endothelial cells to the substrate and the mechanical properties of endothelial cells. However, the accompanying micromechanics and micromotion of endothelial cells were little understood.For the micromotion measurement of the cultured cells, Giaever and Keese (9) developed a morphological biosensor, the electric cell-substrate impedance sensing (ECIS) system. The advantage of this system is that quantitative estimation of cell-to-cell and cell-to-substrate distances can be performed separately and in real time. Atomic force micros...

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Section: Discussionmentioning

confidence: 98%

Measurements of endothelial cell-to-cell and cell-to-substrate gaps and micromechanical properties of endothelial cells during monocyte adhesion

Kataoka

Iwaki

Hashimoto

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

119

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“…One might assume that the endothelium has somehow been dislodged. However, animal models of atherosclerosis, contrary to some early speculations about the effects of hyperlipidemia 53 or smoking, 54,55 have not shown large areas of spontaneous denudation. Moreover, unless active tissue factor is present, it is not obvious that the simple desquamation of endothelium in a high-shear artery would lead to a coagulative and thrombotic process resulting in occlusion.…”

Section: Erosionmentioning

confidence: 91%

Lessons From Sudden Coronary Death

Virmani

Kolodgie

Burke

et al. 2000

ATVB

3,470

1,503

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T his review will reconsider the current paradigm for understanding the critical, final steps in the progression of atherosclerotic lesions. That scheme, largely an outgrowth of observations of autopsy tissues by Davies and colleagues, 1,2 asserts that the cause of death in atherosclerotic coronary artery disease is rupture of an advanced atherosclerotic lesion. Although this assumption may be partially true, recent autopsy studies suggest that it is incomplete. See p 1177To reconsider this paradigm, we reexamined the morphological classification scheme for lesions proposed by the American Heart Association (AHA). 3,4 This scheme is difficult to use for 2 reasons. First, it uses a very long list of roman numerals modified by letter codes that are difficult to remember. Second, it implies an orderly, linear pattern of lesion progression. This tends to be ambiguous, because it is not clear whether there is a single sequence of events during the progression of all lesions. We have therefore tried to devise a simpler classification scheme that is consistent with the AHA categories but is easier to use, able to deal with a wide array of morphological variations, and not overly burdened by mechanistic implications. The Current ParadigmThe current paradigm is based on the belief that type IV lesions, or "atheromas," described by the AHA are stable because the fatty, necrotic core is contained by a smooth muscle cell-rich fibrous cap. Virchow's analysis 5 in 1858 pointed out that historically, the term "atheroma" refers to a dermal cyst ("Grützbalg"), a fatty mass encapsulated within a cap. Extending Virchow's argument, the fibrous cap over the lipid mass of an atherosclerotic plaque is analogous to the capsule containing an abscess, and like an abscess, the plaque can be ruptured. Rupture of the fibrous cap exposes thrombogenic material, initiating platelet aggregation and coagulation in the infiltrating and overlying blood. These thrombotic changes result from activation of the clotting cascade by tissue factor, and further propagation of the thrombosis results from the interaction of platelets with the active thrombogenic matrix. 6 Platelet activation and thrombin formation combined with the evulsion of thrombogenic plaque contents into the lumen then result in sudden occlusion. 7 This widely held concept of atherosclerotic death is based on morphological data from autopsies as well as clinical angiographic studies, in which the presence of surface irregularities has been interpreted as plaque rupture. 8 -10 Previous pathological studies of sudden coronary death have demonstrated evidence of plaque rupture associated with thrombosis in 73% of cases. 2 Of the remaining cases, 8% consist of plaque fissure with intraplaque fibrin deposition and hemorrhage, while 19% show no evidence of thrombi. 2 Consequently, recent reviews of atherosclerosis have uniformly accepted plaque rupture as the critical event leading to coronary artery death. 6

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“…Furthermore, we report that after 24 h of biomechanical stimulation, curved stented pseudovessels show less viable cells with lower increases in cell number and lower NO production than straight stented pseudovessels, indicating a pro-atherosclerotic environment in the curved stented model. It has been shown in other studies that ECs found in the regions of disturbed flow and low WSS display a response characteristic of increased proliferation, including the build-up macrophages, lymphocytes and platelets [2,13,20,21,23,24,[26][27][28]30,55]. Therefore, the altered geometry of the curved pseudovessel and the resulting changes to the flow environment and haemodynamic forces are likely to be responsible for the higher increases in cell number in the rsif.royalsocietypublishing.org J R Soc Interface 10: 20120965 curved unstented models.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, alterations to haemodynamic forces influence the development of vascular pathologies [1][2][3][4][5][6][7][8][9]. Numerous experiments have shown active responses of the vasculature to altered haemodynamic forces, including structural remodelling of the vessel [10 -17], altered cell morphologies [18][19][20][21], proliferation [14,15,22 -24], expression of inflammatory genes ICAM-1 and VCAM-1 [25][26][27][28] and production of nitric oxide (NO) [17,28 -33].…”

Section: Introductionmentioning

confidence: 99%

Comparison of in vitro human endothelial cell response to self-expanding stent deployment in a straight and curved peripheral artery simulator

Ghriallais

McNamara

Bruzzi

2013

J. R. Soc. Interface.

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Haemodynamic forces have a synergistic effect on endothelial cell (EC) morphology, proliferation, differentiation and biochemical expression profiles. Alterations to haemodynamic force levels have been observed at curved regions and bifurcations of arteries but also around struts of stented arteries, and are also known to be associated with various vascular pathologies. Therefore, curvature in combination with stenting might create a proatherosclerotic environment compared with stenting in a straight vessel, but this has never been investigated. The goal of this study was to compare EC morphology, proliferation and differentiation within in vitro models of curved stented peripheral vessel models with those of straight and unstented vessels. These models were generated using both static conditions and also subjected to 24 h of stimulation in a peripheral artery bioreactor. Medicalgrade silicone tubes were seeded with human umbilical vein endothelial cells to produce pseudovessels that were then stented and subjected to 24 h of physiological levels of pulsatile pressure, radial distention and shear stress. Changes in cell number, orientation and nitric oxide (NO) production were assessed in straight, curved, non-stented and stented pseudovessels. We report that curved pseudovessels lead to higher EC numbers with random orientation and lower NO production per cell compared with straight pseudovessels after 24 h of biomechanical stimulation. Both stented curved and stented straight pseudovessels had lower NO production per cell than corresponding unstented pseudovessels. However, in contrast to straight stented pseudovessels, curved stented pseudovessels had fewer viable cells. The results of this study show, for the first time, that the response of the vascular endothelium is dependent on both curvature and stenting combined, and highlight the necessity for future investigations of the effects of curvature in combination with stenting to fully understand effects on the endothelial layer.

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Atherosclerosis-prone branch regions in human aorta: microarchitecture and cell composition of intima

Cited by 32 publications

References 47 publications

Measurements of endothelial cell-to-cell and cell-to-substrate gaps and micromechanical properties of endothelial cells during monocyte adhesion

Measurements of endothelial cell-to-cell and cell-to-substrate gaps and micromechanical properties of endothelial cells during monocyte adhesion

Lessons From Sudden Coronary Death

Comparison of in vitro human endothelial cell response to self-expanding stent deployment in a straight and curved peripheral artery simulator

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