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23 results on '"Wong, Sing Wan"'

5. Manipulation of the nucleoscaffold potentiates cellular reprogramming kinetics

Author

Yang, Benjamin A., primary, da Rocha, André Monteiro, additional, Newton, Isabel, additional, Shcherbina, Anna, additional, Wong, Sing-Wan, additional, Fraczek, Paula M., additional, Larouche, Jacqueline A., additional, Hiraki, Harrison L., additional, Baker, Brendon M., additional, Shin, Jae-Won, additional, Takayama, Shuichi, additional, Thouless, M. D., additional, and Aguilar, Carlos A., additional

Published
2023
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10. Deterministic Single Cell Encapsulation in Asymmetric Microenvironments to Direct Cell Polarity.

Author

Cho, Ik Sung, Gupta, Prerak, Mostafazadeh, Nima, Wong, Sing Wan, Saichellappa, Saiumamaheswari, Lenzini, Stephen, Peng, Zhangli, and Shin, Jae‐Won

Subjects
CELL polarity, CELL-matrix adhesions, MESENCHYMAL stem cells, CELL size, CELL populations, CELL adhesion
Abstract

Various signals in tissue microenvironments are often unevenly distributed around cells. Cellular responses to asymmetric cell‐matrix adhesion in a 3D space remain generally unclear and are to be studied at the single‐cell resolution. Here, the authors developed a droplet‐based microfluidic approach to manufacture a pure population of single cells in a microscale layer of compartmentalized 3D hydrogel matrices with a tunable spatial presentation of ligands at the subcellular level. Cells elongate with an asymmetric presentation of the integrin adhesion ligand Arg‐Gly‐Asp (RGD), while cells expand isotropically with a symmetric presentation of RGD. Membrane tension is higher on the side of single cells interacting with RGD than on the side without RGD. Finite element analysis shows that a non‐uniform isotropic cell volume expansion model is sufficient to recapitulate the experimental results. At a longer timescale, asymmetric ligand presentation commits mesenchymal stem cells to the osteogenic lineage. Cdc42 is an essential mediator of cell polarization and lineage specification in response to asymmetric cell‐matrix adhesion. This study highlights the utility of precisely controlling 3D ligand presentation around single cells to direct cell polarity for regenerative engineering and medicine. [ABSTRACT FROM AUTHOR]

Published
2023
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12. Cell–Matrix Interactions Regulate Functional Extracellular Vesicle Secretion from Mesenchymal Stromal Cells

Author

Lenzini, Stephen, primary, Debnath, Koushik, additional, Joshi, Jagdish C., additional, Wong, Sing Wan, additional, Srivastava, Kriti, additional, Geng, Xue, additional, Cho, Ik Sung, additional, Song, Angela, additional, Bargi, Raymond, additional, Lee, James C., additional, Mo, Gary C.H., additional, Mehta, Dolly, additional, and Shin, Jae-Won, additional

Published
2021
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21. Promyelocytic Leukemia (PML) Protein Plays Important Roles in Regulating Cell Adhesion, Morphology, Proliferation and Migration

Author

Tang, Mei Kuen, primary, Liang, Yong Jia, additional, Chan, John Yeuk Hon, additional, Wong, Sing Wan, additional, Chen, Elve, additional, Yao, Yao, additional, Gan, Jingyi, additional, Xiao, Lihai, additional, Leung, Hin Cheung, additional, Kung, Hsiang Fu, additional, Wang, Hua, additional, and Lee, Kenneth Ka Ho, additional

Published
2013
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22. Programmable microencapsulation for enhanced mesenchymal stem cell persistence and immunomodulation

Author

Mao, Angelo S., Ozkale, Berna, Shah, Nisarg J., Vining, Kyle H., Descombes, Tiphaine, Zhang, Liyuan, Tringides, Christina M., Wong, Sing-Wan, Shin, Jae-Won, Scadden, David T., Weitz, David A., and Mooney, David J.

Subjects
msc, niche, immune modulation, host, graft failure, microfluidics, regenerative medicine, alginate, survival, biomaterials, stromal cells, transplantation, linking
Abstract

Mesenchymal stem cell (MSC) therapies demonstrate particular promise in ameliorating diseases of immune dysregulation but are hampered by short in vivo cell persistence and inconsistencies in phenotype. Here, we demonstrate that biomaterial encapsulation into alginate using a microfluidic device could substantially increase in vivo MSC persistence after intravenous (i.v.) injection. A combination of cell cluster formation and subsequent cross-linking with polylysine led to an increase in injected MSC half-life by more than an order of magnitude. These modifications extended persistence even in the presence of innate and adaptive immunity-mediated clearance. Licensing of encapsulated MSCs with inflammatory cytokine pretransplantation increased expression of immunomodulatory-associated genes, and licensed encapsulates promoted repopulation of recipient blood and bone marrow with allogeneic donor cells after sublethal irradiation by a similar to 2-fold increase. The ability of microgel encapsulation to sustain MSC survival and increase overall immunomodulatory capacity may be applicable for improving MSC therapies in general.

23. Manipulation of the nucleoscaffold potentiates cellular reprogramming kinetics.

Author

Yang BA, da Rocha AM, Newton I, Shcherbina A, Wong SW, Fraczek PM, Larouche JA, Hiraki HL, Baker BM, Shin JW, Takayama S, Thouless MD, and Aguilar CA

Abstract

Somatic cell fate is an outcome set by the activities of specific transcription factors and the chromatin landscape and is maintained by gene silencing of alternate cell fates through physical interactions with the nuclear scaffold. Here, we evaluate the role of the nuclear scaffold as a guardian of cell fate in human fibroblasts by comparing the effects of transient loss (knockdown) and mutation (progeria) of functional Lamin A/C, a core component of the nuclear scaffold. We observed that Lamin A/C deficiency or mutation disrupts nuclear morphology, heterochromatin levels, and increases access to DNA in lamina-associated domains. Changes in Lamin A/C were also found to impact the mechanical properties of the nucleus when measured by a microfluidic cellular squeezing device. We also show that transient loss of Lamin A/C accelerates the kinetics of cellular reprogramming to pluripotency through opening of previously silenced heterochromatin domains while genetic mutation of Lamin A/C into progerin induces a senescent phenotype that inhibits the induction of reprogramming genes. Our results highlight the physical role of the nuclear scaffold in safeguarding cellular fate., Competing Interests: Competing interests The authors declare no competing interests.

Published
2023
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