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134 results on '"Lee, Winston Y."'

6. Multiparametric MRI to quantify disease and treatment response in mice with myeloproliferative neoplasms

Author

Robison, Tanner H., primary, Solipuram, Manisha, additional, Heist, Kevin, additional, Amouzandeh, Ghoncheh, additional, Lee, Winston Y., additional, Humphries, Brock A., additional, Buschhaus, Johanna M., additional, Bevoor, Avinash, additional, Zhang, Anne, additional, Luker, Kathryn E., additional, Pettit, Kristen, additional, Talpaz, Moshe, additional, Malyarenko, Dariya, additional, Chenevert, Thomas L., additional, Ross, Brian D., additional, and Luker, Gary D., additional

Published
2022
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10. Upregulation of CD47 Expression in De Novo Diffuse Large B-Cell Lymphoma Is More Frequent in Activated B-Cell Type

Author

Lee, Winston Y, primary, Perry, Anamarija M., additional, Azcutia, Vero, additional, Herrera, Alex F., additional, Skrabek, Pamela, additional, Jackson, Ryan, additional, Pillai, Raju, additional, Bedell, Victoria, additional, Brazil, Jennifer, additional, Murata-Collins, Joyce, additional, Chan, Wing C., additional, Weisenburger, Dennis D., additional, Parkos, Charles, additional, and Song, Joo Y., additional

Published
2021
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21. Contributors

Author

Aster, Jon C., primary, Chen, Benjamin J., additional, Drage, Michael G., additional, Elco, Christopher P., additional, Evans, Andrew G., additional, Hwang, Dick G., additional, Kondratiev, Svetlana, additional, Kutok, Jeffery L., additional, Lee, Winston Y., additional, Mandelker, Diana, additional, Meserve, Emily E.K., additional, Morgan, Elizabeth A., additional, Pecora, Nicole, additional, Pillai, Vinodh, additional, Pozdnyakova, Olga, additional, and Stonecypher, Mark, additional

Published
2013
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28. Ribosome Levels Selectively Regulate Translation and Lineage Commitment in Human Hematopoiesis

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Khajuria, Rajiv K., Munschauer, Mathias, Ulirsch, Jacob C., Fiorini, Claudia, Ludwig, Leif S., McFarland, Sean K., Abdulhay, Nour J., Specht, Harrison, Keshishian, Hasmik, Mani, Denkanikota R, Jovanovic, Marko, Ellis, Steven R., Fulco, Charles P., Engreitz, Jesse Michael, Schutz, Sabina, Lian, John, Gripp, Karen W., Weinberg, Olga K., Pinkus, Geraldine S., Gehrke, Lee, Regev, Aviv, Lander, Eric Steven, Gazda, Hanna T., Lee, Winston Y., Panse, Vikram G., Sankaran, Vijay G., Carr, Steven A, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Khajuria, Rajiv K., Munschauer, Mathias, Ulirsch, Jacob C., Fiorini, Claudia, Ludwig, Leif S., McFarland, Sean K., Abdulhay, Nour J., Specht, Harrison, Keshishian, Hasmik, Mani, Denkanikota R, Jovanovic, Marko, Ellis, Steven R., Fulco, Charles P., Engreitz, Jesse Michael, Schutz, Sabina, Lian, John, Gripp, Karen W., Weinberg, Olga K., Pinkus, Geraldine S., Gehrke, Lee, Regev, Aviv, Lander, Eric Steven, Gazda, Hanna T., Lee, Winston Y., Panse, Vikram G., Sankaran, Vijay G., and Carr, Steven A

Abstract

Blood cell formation is classically thought to occur through a hierarchical differentiation process, although recent studies have shown that lineage commitment may occur earlier in hematopoietic stem and progenitor cells (HSPCs). The relevance to human blood diseases and the underlying regulation of these refined models remain poorly understood. By studying a genetic blood disorder, Diamond-Blackfan anemia (DBA), where the majority of mutations affect ribosomal proteins and the erythroid lineage is selectively perturbed, we are able to gain mechanistic insight into how lineage commitment is programmed normally and disrupted in disease. We show that in DBA, the pool of available ribosomes is limited, while ribosome composition remains constant. Surprisingly, this global reduction in ribosome levels more profoundly alters translation of a select subset of transcripts. We show how the reduced translation of select transcripts in HSPCs can impair erythroid lineage commitment, illuminating a regulatory role for ribosome levels in cellular differentiation. A global reduction in ribosome levels in Diamond-Blackfan anemia profoundly alters translation of a select subset of transcripts, thereby impeding erythroid lineage commitment. Keyword: hematopoiesis; lineage commitment; GATA1; genetics; ribosome; translation; Diamond-Blackman anemia; erythropoiesis, National Institutes of Health (U.S.) (Grants R01 DK103794), National Institutes of Health (U.S.) (Grant R33 HL120791)

Published
2019

29. Ribosome Levels Selectively Regulate Translation and Lineage Commitment in Human Hematopoiesis

Author

Khajuria, Rajiv K., primary, Munschauer, Mathias, additional, Ulirsch, Jacob C., additional, Fiorini, Claudia, additional, Ludwig, Leif S., additional, McFarland, Sean K., additional, Abdulhay, Nour J., additional, Specht, Harrison, additional, Keshishian, Hasmik, additional, Mani, D.R., additional, Jovanovic, Marko, additional, Ellis, Steven R., additional, Fulco, Charles P., additional, Engreitz, Jesse M., additional, Schütz, Sabina, additional, Lian, John, additional, Gripp, Karen W., additional, Weinberg, Olga K., additional, Pinkus, Geraldine S., additional, Gehrke, Lee, additional, Regev, Aviv, additional, Lander, Eric S., additional, Gazda, Hanna T., additional, Lee, Winston Y., additional, Panse, Vikram G., additional, Carr, Steven A., additional, and Sankaran, Vijay G., additional

Published
2018
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31. A B Cell Regulome Links Notch to Downstream Oncogenic Pathways in Small B Cell Lymphomas

Author

Ryan, Russell J.H., primary, Petrovic, Jelena, additional, Rausch, Dylan M., additional, Zhou, Yeqiao, additional, Lareau, Caleb A., additional, Kluk, Michael J., additional, Christie, Amanda L., additional, Lee, Winston Y., additional, Tarjan, Daniel R., additional, Guo, Bingqian, additional, Donohue, Laura K.H., additional, Gillespie, Shawn M., additional, Nardi, Valentina, additional, Hochberg, Ephraim P., additional, Blacklow, Stephen C., additional, Weinstock, David M., additional, Faryabi, Robert B., additional, Bernstein, Bradley E., additional, Aster, Jon C., additional, and Pear, Warren S., additional

Published
2017
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34. Neutrophil-mediated Activation of Epithelial Protease-Activated Receptors-1 and -2 Regulates Barrier Function and Transepithelial Migration1

Author

Chin, Alex C., Lee, Winston Y., Nusrat, Asma, Vergnolle, Nathalie, and Parkos, Charles A.

Subjects
Cathepsin G, Chemotactic Factors, Pancreatic Elastase, Neutrophils, Myeloblastin, Serine Endopeptidases, Inflammatory Bowel Diseases, Cathepsins, Article, Coculture Techniques, Permeability, Substrate Specificity, Tight Junctions, Gene Expression Regulation, Neutrophil Infiltration, Cell Movement, Humans, Receptor, PAR-2, Receptor, PAR-1, Intestinal Mucosa, Cells, Cultured, Signal Transduction
Abstract

Neutrophil (PMN) infiltration and associated release of serine proteases contribute to epithelial injury during active phases of mucosal disorders such as inflammatory bowel disease. Previous studies have demonstrated that PMN contact with basolateral surfaces of intestinal epithelial cells in the presence of a chemoattractant results in disruption of barrier function even without transmigration. Similarly, serine protease-mediated activation of epithelial protease-activated receptors (PARs) has been shown to increase permeability. In this study, we assessed whether transmigrating PMNs can regulate barrier function through epithelial PAR activation. Transepithelial resistance (TER) decreased significantly after PMN contact with basolateral surfaces of T84 monolayers or after incubation with PMN elastase and proteinase-3, but not cathepsin G. Inhibition of PMN serine proteases, but not selective inhibition of elastase or cathepsin G, prevented the fall in TER induced by PMN contact and blocked PMN transepithelial migration. Basolateral, but not apical, PAR-1 and -2 activation with selective agonists also decreased TER. PAR-1 and -2 were localized intracellularly and in close proximity to lateral surfaces beneath tight junctions, and expression was increased in colonic mucosa from individuals with Crohn's disease. Combined, but not individual, transfection with small interfering RNAs targeted against epithelial PAR-1 and -2, prevented the fall in TER induced by PMN contact. Furthermore, basolateral PAR-1 and -2 activation induced phosphorylation of myosin L chain kinase and regulatory myosin L chain. Lastly, epithelial PAR-1 and -2 knockdown decreased the rate of PMN transepithelial migration. These results suggest that protease-mediated epithelial PAR-1 and -2 activation, by migrating PMNs, induces signaling events that increase epithelial permeability thereby facilitates PMN transepithelial migration.

Published
2008

35. Annexin A1 Regulates Intestinal Mucosal Injury, Inflammation, and Repair1

Author

Babbin, Brian A., Laukoetter, Mike G., Nava, Porfirio, Koch, Stefan, Lee, Winston Y., Capaldo, Christopher T., Peatman, Eric, Severson, Eric A., Flower, Roderick J., Perretti, Mauro, Parkos, Charles A., and Nusrat, Asma

Subjects
Mice, Knockout, endocrine system, Mice, Inbred BALB C, Wound Healing, Dextran Sulfate, Colitis, Severity of Illness Index, Article, Mice, Animals, Female, Genetic Predisposition to Disease, Inflammation Mediators, Intestinal Mucosa, Annexin A1
Abstract

During mucosal inflammation, a complex array of proinflammatory and protective mechanisms regulates inflammation and severity of injury. Secretion of anti-inflammatory mediators is a mechanism that is critical in controlling inflammatory responses and promoting epithelial restitution and barrier recovery. AnxA1 is a potent anti-inflammatory protein that has been implicated to play a critical immune regulatory role in models of inflammation. Although AnxA1 has been shown to be secreted in intestinal mucosal tissues during inflammation, its potential role in modulating the injury/inflammatory response is not understood. In this study, we demonstrate that AnxA1-deficient animals exhibit increased susceptibility to dextran sulfate sodium (DSS)-induced colitis with greater clinical morbidity and histopathologic mucosal injury. Furthermore, impaired recovery following withdrawal of DSS administration was observed in AnxA1 (-/-) animals compared with wild-type (WT) control mice that was independent of inflammatory cell infiltration. Since AnxA1 exerts its anti-inflammatory properties through stimulation of ALX/FPRL-1, we explored the role of this receptor-ligand interaction in regulating DSS-induced colitis. Interestingly, treatment with an ALX/FPRL-1 agonist, 15-epi-lipoxin A4 reversed the enhanced sensitivity of AnxA1 (-/-) mice to DSS colitis. In contrast, 15-epi-lipoxin A4 did not significantly improve the severity of disease in WT animals. Additionally, differential expression of ALX/FPLR-1 in control and DSS-treated WT and AnxA1-deficient animals suggested a potential role for AnxA1 in regulating ALX/FPRL-1 expression under pathophysiological conditions. Together, these results support a role of endogenous AnxA1 in the protective and reparative properties of the intestinal mucosal epithelium.

Published
2008

37. Interferon-gamma regulates intestinal epithelial homeostasis through converging beta-catenin signaling pathways

Author

Nava, Porfirio, Koch, Stefan, Laukoetter, Mike G., Lee, Winston Y., Kolegraff, Keli, Capaldo, Christopher T., Beeman, Neal, Addis, Caroline, Gerner-Smidt, Kirsten, Neumaier, Irmgard, Skerra, Arne, Li, Linheng, Parkos, Charles A., Nusrat, Asma, Nava, Porfirio, Koch, Stefan, Laukoetter, Mike G., Lee, Winston Y., Kolegraff, Keli, Capaldo, Christopher T., Beeman, Neal, Addis, Caroline, Gerner-Smidt, Kirsten, Neumaier, Irmgard, Skerra, Arne, Li, Linheng, Parkos, Charles A., and Nusrat, Asma

Abstract

Inflammatory cytokines have been proposed to regulate epithelial homeostasis during intestinal inflammation. We report here that interferon-gamma (IFN-gamma) regulates the crucial homeostatic functions of cell proliferation and apoptosis through serine-threonine protein kinase AKT-beta-catenin and Wingless-Int (Wnt)-beta-catenin signaling pathways. Short-term exposure of intestinal epithelial cells to IFN-gamma resulted in activation of beta-catenin through AKT, followed by induction of the secreted Wnt inhibitor Dkk1. Consequently, we observed an increase in Dkk1-mediated apoptosis upon extended IFN-gamma treatment and reduced proliferation through depletion of the Wnt coreceptor LRP6. These effects were enhanced by tumor necrosis factor-alpha (TNF-alpha), suggesting synergism between the two cytokines. Consistent with these results, colitis in vivo was associated with decreased beta-catenin-T cell factor (TCF) signaling, loss of plasma membrane-associated LRP6, and reduced epithelial cell proliferation. Proliferation was partially restored in IFN-gamma-deficient mice. Thus, we propose that IFN-gamma regulates intestinal epithelial homeostasis by sequential regulation of converging beta-catenin signaling pathways., Nava, Porfirio Koch, Stefan Laukoetter, Mike G Lee, Winston Y Kolegraff, Keli Capaldo, Christopher T Beeman, Neal Addis, Caroline Gerner-Smidt, Kirsten Neumaier, Irmgard Skerra, Arne Li, Linheng Parkos, Charles A Nusrat, Asma eng R01 DK059888-09/DK/NIDDK NIH HHS/ R01 DK079392/DK/NIDDK NIH HHS/ R01 DK061379-08/DK/NIDDK NIH HHS/ DK55679/DK/NIDDK NIH HHS/ R29 DK055679/DK/NIDDK NIH HHS/ T32 GM008169/GM/NIGMS NIH HHS/ DK72564/DK/NIDDK NIH HHS/ DK64399/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ R01 DK055679-12/DK/NIDDK NIH HHS/ DK53202/DK/NIDDK NIH HHS/ R24 DK064399/DK/NIDDK NIH HHS/ R24 DK064399-019003/DK/NIDDK NIH HHS/ DK59888/DK/NIDDK NIH HHS/ DK79392/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ R01 DK079392-07/DK/NIDDK NIH HHS/ R24 DK064399-019002/DK/NIDDK NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ DK61379/DK/NIDDK NIH HHS/ R01 DK072564-15/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2010/03/23 06:00 Immunity. 2010 Mar 26;32(3):392-402. doi: 10.1016/j.immuni.2010.03.001. Epub 2010 Mar 18.

Published
2010
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38. Surfactant Protein D (Sp-D) Binds to Membrane-proximal Domain (D3) of Signal Regulatory Protein α (SIRPα), a Site Distant from Binding Domain of CD47, while Also Binding to Analogous Region on Signal Regulatory Protein β (SIRPβ)

Author

Fournier, Bénédicte, primary, Andargachew, Rakieb, additional, Robin, Alexander Z., additional, Laur, Oskar, additional, Voelker, Dennis R., additional, Lee, Winston Y., additional, Weber, Dominique, additional, and Parkos, Charles A., additional

Published
2012
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47. Annexin A1 Regulates Intestinal Mucosal Injury, Inflammation, and Repair

Author

Babbin, Brian A., primary, Laukoetter, Mike G., additional, Nava, Porfirio, additional, Koch, Stefan, additional, Lee, Winston Y., additional, Capaldo, Christopher T., additional, Peatman, Eric, additional, Severson, Eric A., additional, Flower, Roderick J., additional, Perretti, Mauro, additional, Parkos, Charles A., additional, and Nusrat, Asma, additional

Published
2008
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50. JAM-A regulates permeability and inflammation in the intestine in vivo

Author

Laukoetter, Mike G., primary, Nava, Porfirio, additional, Lee, Winston Y., additional, Severson, Eric A., additional, Capaldo, Christopher T., additional, Babbin, Brian A., additional, Williams, Ifor R., additional, Koval, Michael, additional, Peatman, Eric, additional, Campbell, Jacquelyn A., additional, Dermody, Terence S., additional, Nusrat, Asma, additional, and Parkos, Charles A., additional

Published
2007
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