Control of Cell‐Substrate Binding Related to Cell Proliferation Cycle Status Using a Cytocompatible Phospholipid Polymer Bearing Phenylboronic Acid Groups

2021 ◽  
pp. 2000341
Author(s):  
Kazuhiko Ishihara ◽  
Masashi Abe ◽  
Kyoko Fukazawa ◽  
Tomohiro Konno
Author(s):  
Sachi Moriwaki ◽  
Yuta Yoshizaki ◽  
Tomohiro Konno

Reversible and cytocompatible cell immobilization polymer matrix with rapid dissociation rate was prepared by using with a zwitterionic phospholipid polymer bearing phenylboronic acid and poly(vinyl alcohol)(PVA). A reversible and spontaneously...


2002 ◽  
Vol 158 (6) ◽  
pp. 1133-1144 ◽  
Author(s):  
Paola Spessotto ◽  
Francesca Maria Rossi ◽  
Massimo Degan ◽  
Raffaele Di Francia ◽  
Roberto Perris ◽  
...  

Osteoclast (OC) precursors migrate to putative sites of bone resorption to form functionally active, multinucleated cells. The preOC FLG 29.1 cells, known to be capable of irreversibly differentiating into multinucleated OC-like cells, displayed several features of primary OCs, including expression of specific integrins and the hyaluronan (HA) receptor CD44. OC-like FLG 29.1 cells adhered to and extensively migrated through membranes coated with fibronectin, vitronectin, and laminins, but, although strongly binding to HA, totally failed to move on this substrate. Moreover, soluble HA strongly inhibited OC-like FLG 29.1 cell migration on the permissive matrix substrates, and this behavior was dependent on its engagement with CD44, as it was fully restored by function-blocking anti-CD44 antibodies. HA did not modulate the cell–substrate binding affinity/avidity nor the expression levels of the corresponding integrins. MMP-9 was the major secreted metalloproteinase used by OC-like FLG 29.1 cells for migration, because this process was strongly inhibited by both TIMP-1 and GM6001, as well as by MMP-9–specific antisense oligonucleotides. After HA binding to CD44, a strong down-regulation of MMP-9 mRNA and protein was detected. These findings highlight a novel role of the HA–CD44 interaction in the context of OC-like cell motility, suggesting that it may act as a stop signal for bone-resorbing cells.


2016 ◽  
Vol 146 ◽  
pp. 318-325 ◽  
Author(s):  
Di Wu ◽  
Jiebing Yang ◽  
Zhen Xing ◽  
Haobo Han ◽  
Tingting Wang ◽  
...  

2009 ◽  
Vol 1191 ◽  
Author(s):  
Helen J Griffiths ◽  
Charles Andrew Collier ◽  
T William Clyne

AbstractThe strength of adhesion at the cell-substrate interface is an important parameter in the design of many prosthetic implant material surfaces, due to the desire to create and maintain a strong implant-tissue bond. This study focuses on the mechanical strength of the interface and the ease of cell removal from ceramic coatings using normal and shear forces, but also looks at cell proliferation rates on the same series of surfaces. This systematic study of cell proliferation and adhesion has been carried out on a series of oxide coated Ti6Al4V based substrates with a range of surface morphologies and chemistries. Oxide coatings were formed using Plasma Electrolytic Oxidation (the PEO process). Cells were seeded at a low concentration onto substrates and proliferation monitored for up to three weeks. The same cell concentrations were seeded on samples for adhesion testing. These were cultured for a few days to ensure well established adhesion of viable cells. The normal and shear strength of osteoblasts (bone cells) and chondrocytes (cartilage cells) adhered to these substrates was measured using accelerated negative buoyancy within an ultracentrifuge. The variation in proliferation rates on, and adhesive strengths to, the range of coatings, is discussed and related to morphological and chemical differences in the coatings. A comparison is made between the normal and shear strengths of the cell-coating bonds and the differences between the behaviour of the two cell types discussed.


Lab on a Chip ◽  
2017 ◽  
Vol 17 (12) ◽  
pp. 2054-2066 ◽  
Author(s):  
Xudong Zhang ◽  
William Wang ◽  
Fang Li ◽  
Ioana Voiculescu

This paper presents the fabrication and testing of a novel stretchable electric cell–substrate impedance sensing (ECIS) lab on a chip device.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Michaela Schernthaner ◽  
Gerd Leitinger ◽  
Heimo Wolinski ◽  
Sepp D. Kohlwein ◽  
Bettina Reisinger ◽  
...  

Nanostructured substrates have been recognized to initiate transcriptional programs promoting cell proliferation. Specificallyβ-catenin has been identified as transcriptional regulator, activated by adhesion to nanostructures. We set out to identify processes responsible for nanostructure-induced endothelialβ-catenin signaling. Transmission electron microscopy (TEM) of cell contacts to differently sized polyethylene terephthalate (PET) surface structures (ripples with 250 to 300 nm and walls with 1.5 µm periodicity) revealed different patterns of cell-substrate interactions. Cell adhesion to ripples occurred exclusively on ripple peaks, while cells were attached to walls continuously. The Src kinase inhibitor PP2 was active only in cells grown on ripples, while the Abl inhibitors dasatinib and imatinib suppressedβ-catenin translocation on both structures. Moreover, Gd3+sensitive Ca2+entry was observed in response to mechanical stimulation or Ca2+store depletion exclusively in cells grown on ripples. Both PP2 and Gd3+suppressedβ-catenin nuclear translocation along with proliferation in cells grown on ripples but not on walls. Our results suggest that adhesion of endothelial cells to ripple structured PET induces highly specific, interface topology-dependent changes in cellular signalling, characterized by promotion of Gd3+-sensitive Ca2+entry and Src/Abl activation. We propose that these signaling events are crucially involved in nanostructure-induced promotion of cell proliferation.


2017 ◽  
Author(s):  
Sebastian V. Hadjiantoniou ◽  
Maxime Leblanc-Latour ◽  
Maxime Ignacio ◽  
Cory S. Lefevbre ◽  
Gary W. Slater ◽  
...  

ABSTRACTDuring Embryogenesis, cells undergo constant organizational remodelling. Biochemical and biophysical guidance cues act in tandem to guide migration and morphogenesis into distinct cellular patterns. It has been shown that various cell types will express different configurations of cellular adhesion molecules known as cadherins and integrins. Cocultured in vitro experiments have focused on revealing the extensive genetic expression profiles that modulate embryogenesis whilst overlooking the physical cell-cell and cell-substrate interactions that influence organization. We demonstrate that NIH3T3 and MDCK cells undergo a spontaneous phase separation when cocultured in vitro and that this phenomenon occurs through purely physical binding energies. A Monte Carlo simulation model of a mixture of cells with different cell-cell and cell-substrate binding energies reveals that the spontaneous phase separation occurs due to the minimization of interfacial free energy within the system. Cell-cell and cell-substrate binding plays a critical role in cell organization and is capable of phase separating different populations of cells in vitro.


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