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530 results on '"Wong, Victor W."'

2. Multiple Subsets of Brain Tumor Initiating Cells Coexist in Glioblastoma

Author

Rennert, Robert C, Achrol, Achal S, Januszyk, Michael, Kahn, Suzana A, Liu, Tiffany T, Liu, Yi, Sahoo, Debashis, Rodrigues, Melanie, Maan, Zeshaan N, Wong, Victor W, Cheshier, Samuel H, Chang, Steven D, Steinberg, Gary K, Harsh, Griffith R, and Gurtner, Geoffrey C

Subjects
Biomedical and Clinical Sciences, Immunology, Rare Diseases, Stem Cell Research - Nonembryonic - Human, Brain Cancer, Stem Cell Research, Brain Disorders, Biotechnology, Cancer, Neurosciences, 2.1 Biological and endogenous factors, Underpinning research, 1.1 Normal biological development and functioning, Aetiology, Biomarkers, Tumor, Brain Neoplasms, Cell Line, Tumor, Glioblastoma, Humans, Neoplastic Stem Cells, Phenotype, Single-Cell Analysis, Transcription, Genetic, Brain tumor initiating cells, Microfluidics, Molecular heterogeneity, Biological Sciences, Technology, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences
Abstract

Brain tumor-initiating cells (BTICs) are self-renewing multipotent cells critical for tumor maintenance and growth. Using single-cell microfluidic profiling, we identified multiple subpopulations of BTICs coexisting in human glioblastoma, characterized by distinct surface marker expression and single-cell molecular profiles relating to divergent bulk tissue molecular subtypes. These data suggest BTIC subpopulation heterogeneity as an underlying source of intra-tumoral bulk tissue molecular heterogeneity, and will support future studies into BTIC subpopulation-specific therapies. Stem Cells 2016;34:1702-1707.

Published
2016

12. Nanotechnology in bone tissue engineering

Author

Walmsley, Graham G., McArdle, Adrian, Tevlin, Ruth, Momeni, Arash, Atashroo, David, Hu, Michael S., Feroze, Abdullah H., Wong, Victor W., Lorenz, Peter H., Longaker, Michael T., and Wan, Derrick C.

Published
2015
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15. Transdermal deferoxamine prevents pressure-induced diabetic ulcers

Author

Duscher, Dominik, Neofytou, Evgenios, Wong, Victor W., Maan, Zeshaan N., Rennert, Robert C., Inayathullah, Mohammed, Januszyk, Michael, Rodrigues, Melanie, Malkovskiy, Andrey V., Whitmore, Arnetha J., Walmsley, Graham G., Galvez, Michael G., Whittam, Alexander J., Brownlee, Michael, Rajadas, Jayakumar, and Gurtner, Geoffrey C.

Published
2015

17. Mechanotransduction and fibrosis

Author

Duscher, Dominik, Maan, Zeshaan N., Wong, Victor W., Rennert, Robert C., Januszyk, Michael, Rodrigues, Melanie, Hu, Michael, Whitmore, Arnetha J., Whittam, Alexander J., Longaker, Michael T., and Gurtner, Geoffrey C.

Published
2014
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40. Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling

Author

Wong, Victor W., Rustad, Kristine C., Akaishi, Satoshi, Sorkin, Michael, Glotzbach, Jason P., Januszyk, Michael, Nelson, Emily R., Levi, Kemal, Paterno, Josemaria, Vial, Ivan N., Kuang, Anna A., Longaker, Michael T., and Gurtner, Geoffrey C.

Subjects
Fibrosis -- Development and progression -- Research, Gene expression -- Research, Phosphotransferases -- Physiological aspects -- Research, Biological sciences, Health
Abstract

Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood1. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK) (1,2). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders (3-5). Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK-ERK-MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation., Traditional cytokine-based paradigms for fibrosis largely overlook the role of cell-matrix interactions and physical cues in disease pathogenesis (4-7). However, clinicians and anatomists have suspected for over a century that [...]

Published
2012
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