scholarly journals Endothelialized silicone aneurysm models for in vitro evaluation of flow diverters

2020 ◽  
pp. neurintsurg-2020-016859
Author(s):  
Alyssa McCulloch ◽  
Ashley Turcott ◽  
Gabriella Graham ◽  
Sergey Frenklakh ◽  
Kristen O'Halloran Cardinal
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Flow Diverter ◽  
In Vitro Models ◽  
Cell Coverage ◽  
Platelet Endothelial Cell Adhesion ◽  
Umbilical Vein Endothelial Cells ◽  
Over Time

ObjectiveThe goal of this work was to endothelialize silicone aneurysm tubes for use as in vitro models for evaluating endothelial cell interactions with neurovascular devices. The first objective was to establish consistent and confluent endothelial cell linings and to evaluate the silicone vessels over time. The second objective was to use these silicone vessels for flow diverter implantation and assessment.MethodsSilicone aneurysm tubes were coated with fibronectin and placed into individual bioreactor systems. Human umbilical vein endothelial cells were deposited within tubes to create silicone vessels, then cultivated on a peristaltic pump and harvested at 2, 5, 7, or 10 days to evaluate the endothelial cell lining. A subset of silicone aneurysm vessels was used for flow diverter implantation, and evaluated for cell coverage over device struts at 3 or 7 days after deployment.ResultsSilicone vessels maintained confluent, PECAM-1 (platelet endothelial cell adhesion molecule 1) positive endothelial cell linings over time. These vessels facilitated and withstood flow diverter implantation, with robust cell linings disclosed after device deployment. Additionally, the endothelial cells responded to implanted devices through coverage of the flow diverter struts with increased cell coverage over the aneurysm seen at 7 days after deployment as compared with 3 days.ConclusionsSilicone aneurysm models can be endothelialized and successfully maintained in vitro over time. Furthermore, these silicone vessels can be used for flow diverter implantation and assessment.

scholarly journals Thrombin-induced gap formation in confluent endothelial cell monolayers in vitro

Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 549-556 ◽  
Author(s):  
M Laposata ◽  
DK Dovnarsky ◽  
HS Shin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Gap Formation ◽  
Culture Dish ◽  
Cell Monolayers ◽  
Umbilical Vein Endothelial Cells

Abstract When thrombin is incubated with confluent monolayers of human umbilical vein endothelial cells in vitro, there is a change in the shape of the endothelial cells that results in gaps in the monolayer, disrupting the integrity of the endothelium and exposing the subendothelium. Using a grid assay to measure this phenomenon, we observed that up to 80% of the surface area once covered by cells was uncovered after a 15-min incubation with 10(-2) U/ml (10(-10)M) thrombin. The effect was apparent within 2 min and did not remove cells from the surface of the culture dish. The gaps in the monolayer completely disappeared within 2 hr after exposure to thrombin. The effect of thrombin was inhibited by preincubation of thrombin with hirudin or antithrombin III plus heparin or by preincubation of the monolayers with dibutyryl cyclic adenosine monophosphate (dbcAMP). Histamine also induced gap formation in endothelial cell monolayers. Both pyrilamine and cimetidine prevented the histamine-induced effect, but they had no effect on thrombin- induced gap formation. Intact monolayers were not disrupted by bradykinin, serotonin, C5a, or C3a. Our results suggest that small amounts of thrombin can induce repeated and transient exposure of the subendothelium, a situation believed to be conducive to atherogenesis and thrombosis.

Modulation Of PGI2-Like Activity Of Human Endothelial Cells By An Extracellular Collagen Matrix

1981 ◽  
Author(s):  
K M Spiegel ◽  
S F Mohammad ◽  
H Y K Chuang ◽  
R G Mason
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Collagen Matrix ◽  
Significant Loss ◽  
Experimental Conditions ◽  
Cell Lysates ◽  
Collagen Coating ◽  
Umbilical Vein Endothelial Cells

Human umbilical vein endothelial cells were grown on several artificial matrices including collagen and on unmodified plastic dishes. Freeze thaw preparations of confluent monolayer endothelial cell cultures were assayed for PGI2-like activity by testing for inhibition of platelet a88regation. The cells grown on a collagen matrix expressed slightly less PGI2-like activity initially compared to the cells grown on plastic. When the PGI2like activity of the cell lysates was examined over a period of three hours after the initial preparation, endothelial cells grown on a collagen matrix exhibited a more rapid loss of activity. Preliminary quantitative evaluations suggest that lysates derived from cells grown on unmodified plastic retained 75% PGI2 like activity at 15 min, at which point collagen grown cells exhibited essentially no PGI2-like activity. Furthermore, as shown in the figure, under identical experimental conditions, cell lysates obtained from endothelial cells grown on unmodified plastic continued to express approximately 50% of the initial PGI2-like activity after one hour. Since addition of purified PGI2 or cell lysates in vitro to the collagen coating used as tissue culture substrate failed to cause any significant loss of platelet aggregation inhibitory activity beyond the normal rate of decay of PGI2 it appears likely that the reduction of PGI2-like activity may be associated with changes in the substrate collagen, possibly effected by the endothelial cell layer. Alternatively, the reduction of activity may be related to differences in the endothelial cells caused by growth on the collagen substrate.

scholarly journals Immunosuppressive nano-therapeutic micelles downregulate endothelial cell inflammation and immunogenicity

RSC Advances ◽  
2015 ◽  
Vol 5 (54) ◽  
pp. 43552-43562 ◽  
Author(s):  
Satish N. Nadig ◽  
Suraj K. Dixit ◽  
Natalie Levey ◽  
Scott Esckilsen ◽  
Kayla Miller ◽  
...  
Keyword(s):  
Immune Response ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Perfusion Solution ◽  
Umbilical Vein Endothelial Cells

Targeted micelles containing rapamycin (TRaM) suppressed the immune response of IL-8 in oxidatively stressed human umbilical vein endothelial cellsin vitro(a) and accumulated in aorta grafts for transplantation after 6 hours in cold perfusion solution (b).

scholarly journals Thrombin-induced gap formation in confluent endothelial cell monolayers in vitro

Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 549-556 ◽  
Author(s):  
M Laposata ◽  
DK Dovnarsky ◽  
HS Shin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Gap Formation ◽  
Culture Dish ◽  
Cell Monolayers ◽  
Umbilical Vein Endothelial Cells

When thrombin is incubated with confluent monolayers of human umbilical vein endothelial cells in vitro, there is a change in the shape of the endothelial cells that results in gaps in the monolayer, disrupting the integrity of the endothelium and exposing the subendothelium. Using a grid assay to measure this phenomenon, we observed that up to 80% of the surface area once covered by cells was uncovered after a 15-min incubation with 10(-2) U/ml (10(-10)M) thrombin. The effect was apparent within 2 min and did not remove cells from the surface of the culture dish. The gaps in the monolayer completely disappeared within 2 hr after exposure to thrombin. The effect of thrombin was inhibited by preincubation of thrombin with hirudin or antithrombin III plus heparin or by preincubation of the monolayers with dibutyryl cyclic adenosine monophosphate (dbcAMP). Histamine also induced gap formation in endothelial cell monolayers. Both pyrilamine and cimetidine prevented the histamine-induced effect, but they had no effect on thrombin- induced gap formation. Intact monolayers were not disrupted by bradykinin, serotonin, C5a, or C3a. Our results suggest that small amounts of thrombin can induce repeated and transient exposure of the subendothelium, a situation believed to be conducive to atherogenesis and thrombosis.

scholarly journals Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

2017 ◽  
Vol 114 (8) ◽  
pp. 1940-1945 ◽  
Author(s):  
Li Shen ◽  
Zhenyu Diao ◽  
Hai-Xiang Sun ◽  
Gui-Jun Yan ◽  
Zhiqun Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Umbilical Vein ◽  
Normal Pregnancy ◽  
Uterine Wall ◽  
High Dose ◽  
Endothelial Cell Activation ◽  
Umbilical Vein Endothelial Cells

Preeclampsia (PE) is initiated by abnormal placentation in the early stages of pregnancy, followed by systemic activation of endothelial cells of the maternal small arterioles in the late second or third trimester (TM) of pregnancy. During normal pregnancy, placental cytotrophoblasts (CTBs) invade the maternal uterine wall and spiral arteries, whereas this process is interrupted in PE. However, it is not known how the malformed placenta triggers maternal endothelial crisis and the associated manifestations. Here, we have focused on the association of CD81 with PE. CD81, a member of the tetraspanin superfamily, plays significant roles in cell growth, adhesion, and motility. The function of CD81 in human placentation and its association with pregnancy complications are currently unknown. In the present study, we have demonstrated that CD81 was preferentially expressed in normal first TM placentas and progressively down-regulated with gestation advance. In patients with early-onset severe PE (sPE), CD81 expression was significantly up-regulated in syncytiotrophoblasts (STBs), CTBs and the cells in the villous core. In addition, high levels of CD81 were observed in the maternal sera of patients with sPE. Overexpressing CD81 in CTBs significantly decreased CTB invasion, and culturing primary human umbilical vein endothelial cells (HUVECs) in the presence of a high dose of exogenous CD81 resulted in interrupted angiogenesis and endothelial cell activation in vitro. Importantly, the phenotype of human PE was mimicked in the CD81-induced rat model.

Induction and Suppression of Endothelial Cell Apoptosis by Sphingolipids: A Possible In Vitro Model for Cell-Cell Interactions Between Platelets and Endothelial Cells

Blood ◽  
1999 ◽  
Vol 93 (12) ◽  
pp. 4293-4299 ◽  
Author(s):  
Nobuo Hisano ◽  
Yutaka Yatomi ◽  
Kaneo Satoh ◽  
Shigeo Akimoto ◽  
Masako Mitsumata ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cell Interaction ◽  
Dependent Manner ◽  
Survival Factor ◽  
Highly Active ◽  
Sphingosine 1 Phosphate ◽  
Umbilical Vein Endothelial Cells

Because sphingosine (Sph) is actively incorporated into platelets and rapidly converted to sphingosine 1-phosphate (Sph-1-P), which is then released extracellularly, it is important to study the effects of Sph and Sph-1-P on endothelial cells from the viewpoint of platelet-endothelial cell interaction. In this study, we found that Sph, as well as ceramide, induces apoptosis in human umbilical vein endothelial cells (HUVECs). In contrast, Sph-1-P acts as a HUVEC survival factor; this bioactive lipid was shown to protect HUVECs from apoptosis induced by the withdrawal of growth factors and to stimulate HUVEC DNA synthesis. In metabolic studies, [3H]Sph, incorporated into HUVECs, was converted to [3H]Cer and further to [3H]sphingomyelin in a time-dependent manner, whereas [3H]Sph-1-P formation from [3H]Sph was weak and transient. These findings in HUVECs are very different from those of platelets, which possess a highly active Sph kinase but lack Sph-1-P lyase. As a result, platelets abundantly store Sph-1-P, whereas HUVECs contain much less Sph-1-P. Finally, HUVECs, in contrast to platelets, failed to release Sph-1-P extracellularly, indicating that HUVECs themselves are not able to supply the survival factor Sph-1-P, but receive it from activated platelets. Our results suggest that platelets may maintain the integrity of endothelial cells by incorporating Sph and releasing Sph-1-P.

Induction and Suppression of Endothelial Cell Apoptosis by Sphingolipids: A Possible In Vitro Model for Cell-Cell Interactions Between Platelets and Endothelial Cells

Blood ◽  
1999 ◽  
Vol 93 (12) ◽  
pp. 4293-4299 ◽  
Author(s):  
Nobuo Hisano ◽  
Yutaka Yatomi ◽  
Kaneo Satoh ◽  
Shigeo Akimoto ◽  
Masako Mitsumata ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cell Interaction ◽  
Dependent Manner ◽  
Survival Factor ◽  
Highly Active ◽  
Sphingosine 1 Phosphate ◽  
Umbilical Vein Endothelial Cells

Abstract Because sphingosine (Sph) is actively incorporated into platelets and rapidly converted to sphingosine 1-phosphate (Sph-1-P), which is then released extracellularly, it is important to study the effects of Sph and Sph-1-P on endothelial cells from the viewpoint of platelet-endothelial cell interaction. In this study, we found that Sph, as well as ceramide, induces apoptosis in human umbilical vein endothelial cells (HUVECs). In contrast, Sph-1-P acts as a HUVEC survival factor; this bioactive lipid was shown to protect HUVECs from apoptosis induced by the withdrawal of growth factors and to stimulate HUVEC DNA synthesis. In metabolic studies, [3H]Sph, incorporated into HUVECs, was converted to [3H]Cer and further to [3H]sphingomyelin in a time-dependent manner, whereas [3H]Sph-1-P formation from [3H]Sph was weak and transient. These findings in HUVECs are very different from those of platelets, which possess a highly active Sph kinase but lack Sph-1-P lyase. As a result, platelets abundantly store Sph-1-P, whereas HUVECs contain much less Sph-1-P. Finally, HUVECs, in contrast to platelets, failed to release Sph-1-P extracellularly, indicating that HUVECs themselves are not able to supply the survival factor Sph-1-P, but receive it from activated platelets. Our results suggest that platelets may maintain the integrity of endothelial cells by incorporating Sph and releasing Sph-1-P.

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