Expression of MacMARCKS Restores Cell Adhesion to ICAM-1-Coated Surface

SummaryPlatelet adhesion at sites of cardiovascular injury may facilitate leukocyte deposition. We asked if and how platelets enhance lymphocyte adhesion on different subendothelial matrix protein (SEMP)-coated surface at arterial shear stress. Hirudinised whole blood was subjected to an arterial shear rate (500 s−1) in a Cone and Plate(let) analyser (CPA) for 5 minutes using plates coated with bovine serum albumin (BSA), collagen, fibrinogen, von Willebrand factor (vWF), or fibronectin. Platelet and lymphocyte adhesion were monitored by CPA and flow cytometry. Exposure of blood to collagen, fibrinogen, and vWF-coated surfaces induced platelet activation. The most marked effect was seen with collagen-coating, which markedly enhanced the adhesion of all lymphocyte subpopulations compared to BSA-coating. Fibrinogen-coating supported both T and NK cell adhesion, while vWF-coated surface only enhanced NK cell deposition. In contrast, fibronectin enhanced neither platelet activation nor lymphocyte adhesion. Moreover, platelets preferentially facilitated adhesion of large CD4+ and CD8+ T cells and NK cells, and of small B cells. Enhanced cell adhesion of larger lymphocytes was associated with elevated platelet conjugation and higher lymphocyte expression of PSGL-1, Mac-1, and CD40L. The enhancement of lymphocyte adhesion was totally platelet-dependent, and was abolished in platelet-depleted blood. Moreover, blockade of the platelet adhesion molecules P-selectin, GPIIb/IIIa, and CD40L attenuated platelet-dependent lymphocyte deposition. In conclusion, platelets support lymphocyte adhesion on SEMP-coated surfaces under arterial shear. The enhancement is selective for large T and NK cells and small B cells.

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Peptide Antagonists for P-selectin Discriminate between Sulfatide-Dependent Platelet Aggregation and PSGL-1-Mediated Cell Adhesion

Journal of Clinical Medicine ◽

10.3390/jcm8081266 ◽

2019 ◽

Vol 8 (8) ◽

pp. 1266 ◽

Cited By ~ 2

Author(s):

Suzanne J.A. Korporaal ◽

Tom J.M. Molenaar ◽

Bianca C.H. Lutters ◽

Illiana Meurs ◽

Sandra Drost-Verhoef ◽

...

Keyword(s):

Cell Adhesion ◽

Platelet Aggregation ◽

Hot Spots ◽

Inhibitory Concentration ◽

Platelet Surface ◽

Core Motif ◽

Multiple Binding ◽

Binding Pockets ◽

Dependent Cell ◽

Coated Surface

Background: Membrane-exposed sulfatides are proposed to contribute to P-selectin-dependent platelet aggregation. Here, we demonstrated that P-selectin-mediated platelet aggregation on a collagen-coated surface under flow indeed depended on sulfatides and that this interaction differed considerably from the interaction of P-selectin with P-selectin Glycoprotein Ligand-1 (PSGL-1), which underlies leukocyte-endothelium adhesion. Methods and Results: Upon platelet activation, sulfatides were translocated to the platelet surface to form focal hot-spots. Interestingly, P-selectin was observed to exclusively interact with liposomes with a sulfatide density higher than 21% (w/w), indicating that the binding profile of P-selectin for sulfatide-rich liposomes was dependent on sulfatide density. Sulfatide-liposome binding to P-selectin and sulfatide/P-selectin-dependent platelet aggregation was blunted by peptide antagonists, carrying the EWVDV motif within N-terminal extensions, such as CDVEWVDVSC (half maximal inhibitory concentration IC50 = 0.2 μM), but not by the EWVDV core motif itself (IC50 > 1000 μM), albeit both being equally potent inhibitors of PSGL-1/P-selectin interaction (IC50= 7–12 μM). Conclusions: Our data suggest that the sulfatide/P-selectin interaction implicates multiple binding pockets, which only partly overlap with that of PSGL-1. These observations open ways to selectively interfere with sulfatide/P-selectin-dependent platelet aggregation without affecting PSGL-1-dependent cell adhesion.

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Layer-by-layer siRNA/poly(L-lysine) Multilayers on Polydopamine-coated Surface for Efficient Cell Adhesion and Gene Silencing

Scientific Reports ◽

10.1038/s41598-018-25655-7 ◽

2018 ◽

Vol 8 (1) ◽

Cited By ~ 13

Author(s):

Cheol Am Hong ◽

Ho Yeon Son ◽

Yoon Sung Nam

Keyword(s):

Cell Adhesion ◽

Gene Silencing ◽

Layer By Layer ◽

Coated Surface

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719 Cell adhesion control based on selective hydrophilization of fluorine coated surface

The proceedings of the JSME annual meeting ◽

10.1299/jsmemecjo.2006.5.0_239 ◽

2006 ◽

Vol 2006.5 (0) ◽

pp. 239-240

Author(s):

Katsuya SATO ◽

Yutaka MIKI ◽

Kazuyuki MINAMI

Keyword(s):

Cell Adhesion ◽

Coated Surface ◽

Adhesion Control

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Effect of Collagen Coating on Lipid Accumulation and Differentiation on 3T3-L1 Preadipocyte Treated with Conjugated Linoleic Acid

Key Engineering Materials ◽

10.4028/www.scientific.net/kem.342-343.261 ◽

2007 ◽

Vol 342-343 ◽

pp. 261-264

Author(s):

Hyun Seuk Moon ◽

Hong Gu Lee ◽

Ho Hyun Song ◽

Yun Jaie Choi ◽

Chong Su Cho

Keyword(s):

Cell Adhesion ◽

Linoleic Acid ◽

Good Adhesion ◽

Replacement Strategy ◽

Gpdh Activity ◽

Collagen Coating ◽

Proliferation And Differentiation ◽

Coated Surface ◽

Glycerol 3 Phosphate Dehydrogenase ◽

Adipocyte Precursor

The purpose of this study is to make use of trans10,cis12 CLA (t-CLA) that has potential for proliferation and differentiation to form adipocyte on the collagen-coated surface. Results provided evidences of good adhesion, growth, viability, and differentiation of adipocyte on collagen-coated surface compared with non-coated surface. Also, the results showed that mouse 3T3-L1 preadipocyte can be successfully and reproducibly cultured on the collagen-coated surface, and the adipocyte precursor cells placed on the collagen-coated surface are able to undergo full maturation into adipocytes in the control cells. Moreover, glycerol-3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 preadipocyte cultured on collagen-coated surface with t-CLA was higher than that on polystyrene (PS) surface due to higher cell adhesion and cell viability. These results suggest that collagen coating may provide a promising approach to develop a new adipocyte replacement strategy using CLA.

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Amyloid Aggregates of Smooth-Muscle Titin Impair Cell Adhesion

International Journal of Molecular Sciences ◽

10.3390/ijms22094579 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4579

Author(s):

Alexander G. Bobylev ◽

Roman S. Fadeev ◽

Liya G. Bobyleva ◽

Margarita I. Kobyakova ◽

Yuri M. Shlyapnikov ◽

...

Keyword(s):

Smooth Muscle ◽

Cell Adhesion ◽

Amyloid Β ◽

Force Microscopy ◽

Atomic Force ◽

Amyloid Aggregates ◽

Negative Effect ◽

Coated Surface

Various amyloid aggregates, in particular, aggregates of amyloid β-proteins, demonstrate in vitro and in vivo cytotoxic effects associated with impairment of cell adhesion. We investigated the effect of amyloid aggregates of smooth-muscle titin on smooth-muscle-cell cultures. The aggregates were shown to impair cell adhesion, which was accompanied by disorganization of the actin cytoskeleton, formation of filopodia, lamellipodia, and stress fibers. Cells died after a 72-h contact with the amyloid aggregates. To understand the causes of impairment, we studied the effect of the microtopology of a titin-amyloid-aggregate-coated surface on fibroblast adhesion by atomic force microscopy. The calculated surface roughness values varied from 2.7 to 4.9 nm, which can be a cause of highly antiadhesive properties of this surface. As all amyloids have the similar structure and properties, it is quite likely that the antiadhesive effect is also intrinsic to amyloid aggregates of other proteins. These results are important for understanding the mechanisms of the negative effect of amyloids on cell adhesion.

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Integrin-mediated adhesion in the unicellular holozoan Capsaspora owczarzaki

10.1101/2020.02.27.967653 ◽

2020 ◽

Cited By ~ 1

Author(s):

Helena Parra-Acero ◽

Matija Harcet ◽

Núria Sánchez-Pons ◽

Elena Casacuberta ◽

Nicholas H. Brown ◽

...

Keyword(s):

Cell Adhesion ◽

Comparative Genomic ◽

Adhesion Assay ◽

Cell Matrix ◽

Substrate Adhesion ◽

Cell Substrate ◽

Associated Proteins ◽

Core Components ◽

Coated Surface ◽

Cell Substrate Adhesion

AbstractIn animals, cell-matrix adhesion is mainly mediated by integrins and their associated proteins. Comparative genomic analyses have shown that core components of the integrin adhesome pre-date the emergence of animals, however, whether it mediates cell adhesion in non-metazoan taxa remains unknown. Here, we investigate cell-substrate adhesion in Capsaspora owczarzaki, the closest unicellular relative of animals with the most complete integrin adhesome. Using an adhesion assay, we show that C. owczarzaki adheres to surfaces using actin-dependent filopodia. We show that integrin β2 and its associated protein vinculin localise as distinct patches in the filopodia. We also demonstrate that substrate adhesion and integrin localisation are enhanced by the ligand fibronectin. Finally, using a specific antibody for Integrin β2, we inhibited cell adhesion to a fibronectin-coated surface. Our results show that adhesion to the substrate in C. owczarzaki is mediated by integrins. This suggests that integrin-mediated adhesion pre-dates the emergence of animals.

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