Interaction of soft condensed materials with living cells:  Phenotype/transcriptome correlations for the hydrophobic effect

Allen, Lorcan T.; Fox, Edward J.; Blute, Irena; Kelly, Zoe D.; Rochev, Yuri; Keenan, A. K.; Dawson, Kenneth A.; Gallagher, William M.

doi:10.1073/pnas.1031426100

Cited by 76 publications

(66 citation statements)

References 24 publications

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“…For all media types, increasing the ratio of BAM in the copolymer nanoparticles was shown to cause a decrease in their zeta potential. This increasingly negative value of the zeta potential of the co-polymer particle surface is consistent with the reduced hydrophillicity (as determined by contact angle measurements) as a result of the increased BAM content (Lynch et al, 2005;Allen et al, 2003). A similar trend was observed with all the media tested but was most significant when the nanoparticles were tested in MQ water.…”

Section: Zeta Potential Measurementsupporting

confidence: 78%

Preparation, characterization of NIPAM and NIPAM/BAM copolymer nanoparticles and their acute toxicity testing using an aquatic test battery

Naha¹,

Casey²,

Tenuta

et al. 2009

Aquatic Toxicology

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Section: Zeta Potential Measurementsupporting

confidence: 78%

Preparation, characterization of NIPAM and NIPAM/BAM copolymer nanoparticles and their acute toxicity testing using an aquatic test battery

Naha¹,

Casey²,

Tenuta

et al. 2009

Aquatic Toxicology

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“…The polymer particles were chosen as models for our studies because they are well controlled in size and purity. They have previously been reported to have low toxicity (43,44), and similar particles are currently being investigated as drug delivery devices in vivo (45). They also allow the size (curvature) and hydrophobicity of the nanoparticle surfaces to be varied systematically, allowing elucidation of the control parameters for nucleation and growth in a novel and powerful manner.…”

mentioning

confidence: 99%

Nucleation of protein fibrillation by nanoparticles

Linse

Cabaleiro-Lago

Xue

et al. 2007

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

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810

769

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Nanoparticles present enormous surface areas and are found to enhance the rate of protein fibrillation by decreasing the lag time for nucleation. Protein fibrillation is involved in many human diseases, including Alzheimer's, Creutzfeld-Jacob disease, and dialysis-related amyloidosis. Fibril formation occurs by nucleationdependent kinetics, wherein formation of a critical nucleus is the key rate-determining step, after which fibrillation proceeds rapidly. We show that nanoparticles (copolymer particles, cerium oxide particles, quantum dots, and carbon nanotubes) enhance the probability of appearance of a critical nucleus for nucleation of protein fibrils from human ␤2-microglobulin. The observed shorter lag (nucleation) phase depends on the amount and nature of particle surface. There is an exchange of protein between solution and nanoparticle surface, and ␤2-microglobulin forms multiple layers on the particle surface, providing a locally increased protein concentration promoting oligomer formation. This and the shortened lag phase suggest a mechanism involving surface-assisted nucleation that may increase the risk for toxic cluster and amyloid formation. It also opens the door to new routes for the controlled self-assembly of proteins and peptides into novel nanomaterials.amyloid ͉ nanotoxicology ͉ surface-assisted nucleation

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“…cell adhesion ͉ signaling ͉ osteoblast ͉ mineralization B iomaterial surface chemistry modulates in vitro and in vivo cellular responses, including adhesion, survival, cell cycle progression, and expression of differentiated phenotypes (1)(2)(3)(4)(5)(6)(7)(8). These cell-material interactions regulate cell and host responses to implanted devices, biological integration of biomaterials and tissue-engineered constructs, and the performance of cell arrays and biotechnological cell culture supports (9)(10)(11)(12).…”

mentioning

confidence: 99%

Integrin binding specificity regulates biomaterial surface chemistry effects on cell differentiation

Keselowsky

Collard

Garcı́a

2005

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

618

466

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Biomaterial surface chemistry has profound consequences on cellular and host responses, but the underlying molecular mechanisms remain poorly understood. Using self-assembled monolayers as model biomaterial surfaces presenting well defined chemistries, we demonstrate that surface chemistry modulates osteoblastic differentiation and matrix mineralization independently from alterations in cell proliferation. Surfaces were precoated with equal densities of fibronectin (FN), and surface chemistry modulated FN structure to alter integrin adhesion receptor binding. OH-and NH 2-terminated surfaces up-regulated osteoblast-specific gene expression, alkaline phosphatase enzymatic activity, and matrix mineralization compared with surfaces presenting COOH and CH 3 groups. These surface chemistry-dependent differences in cell differentiation were controlled by binding of specific integrins to adsorbed FN. Function-perturbing antibodies against the central cell binding domain of FN completely inhibited matrix mineralization. Furthermore, blocking antibodies against ␤1 integrin inhibited matrix mineralization on the OH and NH 2 surfaces, whereas function-perturbing antibodies specific for ␤3 integrin increased mineralization on the COOH substrate. These results establish surface-dependent differences in integrin binding as a mechanism regulating differential cellular responses to biomaterial surfaces. This mechanism could be exploited to engineer materials that control integrin binding specificity to elicit desired cellular activities to enhance the integration of biomaterials and improve the performance of biotechnological culture supports.cell adhesion ͉ signaling ͉ osteoblast ͉ mineralization B iomaterial surface chemistry modulates in vitro and in vivo cellular responses, including adhesion, survival, cell cycle progression, and expression of differentiated phenotypes (1-8). These cell-material interactions regulate cell and host responses to implanted devices, biological integration of biomaterials and tissue-engineered constructs, and the performance of cell arrays and biotechnological cell culture supports (9-12). For instance, anionic and neutral hydrophilic surfaces increase macrophage͞ monocyte apoptosis and reduce macrophage fusion to modulate inflammatory responses to implanted materials (8). The effects of biomaterial surface properties on cellular responses are generally attributed to material-dependent differences in adsorbed protein species, concentration, and͞or biological activity. Nonetheless, the molecular mechanisms modulating these substrate-dependent, complex higher-order cellular activities remain poorly understood. This lack of a fundamental understanding of cell-material interactions hinders progress toward the development of synthetic materials that elicit desired cellular responses. Using self-assembled monolayers (SAMs) presenting well defined chemistries as model biomaterial surfaces, we previously showed that surface chemistry modulates the structure and activity of adsorbed fibronectin (FN) (13)...

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Interaction of soft condensed materials with living cells: Phenotype/transcriptome correlations for the hydrophobic effect

Cited by 76 publications

References 24 publications

Preparation, characterization of NIPAM and NIPAM/BAM copolymer nanoparticles and their acute toxicity testing using an aquatic test battery

Preparation, characterization of NIPAM and NIPAM/BAM copolymer nanoparticles and their acute toxicity testing using an aquatic test battery

Nucleation of protein fibrillation by nanoparticles

Integrin binding specificity regulates biomaterial surface chemistry effects on cell differentiation

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