Effect of fibronectin amount and conformation on the strength of endothelial cell adhesion to HEMA/EMA copolymers

Burmeister, Jeffrey S.; Vrany, J. D.; Reichert, William M.; Truskey, George A.

doi:10.1002/(sici)1097-4636(199601)30:1<13::aid-jbm3>3.0.co;2-u

Cited by 73 publications

(38 citation statements)

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“…To confirm these data we carried out experiments in which adhesion of MDA-MB231 cells was prevented by culturing them in poly-HEMA, an inert polymer impeding cell attachment [49]. Our results show that MDA-MB231 cells, cultured in poly-HEMA, grew in cluster and did not present morphological alterations (control cells in Fig.…”

Section: The Effects Of Saha and Trail On Mda-mb231 Cells Cultured Insupporting

confidence: 57%

SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

et al. 2012

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a b s t r a c t SAHA, an inhibitor of histone deacetylase activity, has been shown to sensitize tumor cells to apoptosis induced by TRAIL, a member of TNF-family. In this paper we investigated the effect of SAHA/TRAIL combination in two breast cancer cell lines, the ERaÀpositive MCF-7 and the ERaÀnegative MDA-MB231. Treatment of MDA-MB231 and MCF-7 cells with SAHA in combination with TRAIL caused detachment of cells followed by anoikis, a form of apoptosis which occurs after cell detachment, while treatment with SAHA or TRAIL alone did not produce these effects. The effects were more evident in MDA-MB231 cells, which were chosen for ascertaining the mechanism of SAHA/TRAIL action. Our results show that SAHA decreased the level of c-FLIP, thus favouring the interaction of TRAIL with the specific death receptors DR4 and DR5 and the consequent activation of caspase-8. These effects increased when the cells were treated with SAHA/TRAIL combination. Because z-IEDT-fmk, an inhibitor of caspase-8, prevented both the cleavage of the focal adhesion-kinase FAK and cell detachment, we suggest that activation of caspase-8 can be responsible for both the decrement of FAK and the consequent cell detachment. In addition, treatment with SAHA/TRAIL combination caused dissipation of DJ m , activation of caspase-3 and decrement of both phospho-EGFR and phospho-ERK1/2, a kinase which is involved in the phosphorylation of BimEL. Therefore, co-treatment also induced decrement of phospho-BimEL and a concomitant increase in the dephosphorylated form of BimEL, which plays an important role in the induction of anoikis.Our findings suggest the potential application of SAHA in combination with TRAIL in clinical trials for breast cancer.

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Section: The Effects Of Saha and Trail On Mda-mb231 Cells Cultured Insupporting

confidence: 57%

SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

et al. 2012

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“…Attachment of cells to a surface relies on orientational control of ECM protein surface adsorption and molecule conformation. Interaction between substrate and cells directly influences cell behavior, communicated from membrane (integrin) receptors via cytoskeletal and biochemical networks to influence cell growth, ECM formation and orientation (Mrksich and Whitesides 1996;Burmeister et al 1996;Wilson et al 2001). It has been shown that aggregation of ECM molecules such as collagen is important in formation of a fibrillar network in vivo (Bozec and Horton 2005), though the mechanism is not well understood.…”

Section: Discussionmentioning

confidence: 99%

Influence of Systematically Varied Nano-Scale Topography on Cell Morphology and Adhesion

Heydarkhan‐Hagvall

Choi

Dunn

et al. 2007

Cell Communication & Adhesion

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The types of cell-matrix adhesions and the signals they transduce strongly affect the cellphenotype. We hypothesized that cells sense and respond to the three-dimensionality of their environment, which could be modulated by nano-structures on silicon surfaces. Human foreskin fibroblasts were cultured on nano-structures with different patterns (nano-post and nano-grate) and heights for 3 days. The presence of integrin α 5 ,β 1 , β 3 , paxillin and phosphorylated FAK (pFAK) were detected by western blot and immunofluorescence. Integrin β 3 exhibited stronger signals on nano-grates. pFAK and paxillin were observed as small dot-like patterns on the cellperiphery on nano-posts and as elongated and aligned patterns on nano-grates. Collectively, our observations highlighted the presence of focal (integrin β 1 , β 3 , pFAK, paxillin), fibrillar (integrin α 5 , β 1 ) and 3-D matrix (integrin α 5 , β 1 , paxillin) adhesions on nano-structures. The presented nano-structures offer interesting opportunities to study the interaction of cells with topographical features comparable to the size of extracellular matrix components.

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“…Assuming surface topography and porosity are similar for all surfaces, initial adhesion is determined by the conformation and amount of protein intentionally or unintentionally (from serum), adsorbed on the material surface (which is in turn dependent on underlying material chemistry). Fibronectin produced the highest initial adhesion [121], while at later time points, when cell confluence was attained, no difference was seen on different ECM component coatings [122][123][124][125]. It is worth noting here that many studies on polymer grafts were confounded by variations in graft porosity or surface roughness, which alter the local stress state sensed by the EC.…”

Section: Ec Proliferation and Adhesion On Biomaterialsmentioning

confidence: 99%

The influence of biomaterials on endothelial cell thrombogenicity

2007

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Driven by tissue engineering and regenerative medicine, endothelial cells are being used in combination with biomaterials in a number of applications for the purpose of improving blood compatibility and host integration. Endothelialized vascular grafts are beginning to be used clinically with some success in some centers, while endothelial seeding is being explored as a means of creating a vasculature within engineered tissues. The underlying assumption of this strategy is that when cultured on artificial biomaterials, a confluent layer of endothelial cells maintain their nonthrombogenic phenotype. In this review the existing knowledge base of endothelial cell thrombogenicity cultured on a number of different biomaterials is summarized. The importance of selecting appropriate endpoint measures that are most reflective of overall surface thrombogenicity is the focus of this review. Endothelial cells inhibit thrombosis through three interconnected regulatory systems (1) the coagulation cascade (2) the cellular components of the blood such as leukocytes and platelets and (3) the complement cascade, and also through effects on fibrinolysis and vascular tone, the latter which influences blood flow. Thus, in order to demonstrate the thromobgenic benefit of seeding a biomaterial with EC, the conditions under which EC surfaces are more likely to exhibit lower thrombogenicity than unseeded biomaterial surfaces need to be consistent with the experimental context. The endpoints selected should be appropriate for the dominant thrombotic process that occurs under the given experimental conditions.

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Effect of fibronectin amount and conformation on the strength of endothelial cell adhesion to HEMA/EMA copolymers

Cited by 73 publications

References 1 publication

SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

Influence of Systematically Varied Nano-Scale Topography on Cell Morphology and Adhesion

The influence of biomaterials on endothelial cell thrombogenicity

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