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1,012 results on '"Liu, Fu-Tong"'

203. Allergen-induced airway remodeling is impaired in galectin-3 deficient mice1

Author

Ge, Xiao Na, Bahaie, Nooshin S., Kang, Bit Na, Hosseinkhani, Reza M., Ha, Sung Gil, Frenzel, Elizabeth M., Liu, Fu-Tong, Rao, Savita P., and Sriramarao, P.

Subjects
Chemokine CCL11, Inflammation, Male, Mice, Knockout, Interleukin-13, Ovalbumin, Reverse Transcriptase Polymerase Chain Reaction, Galectin 3, Blotting, Western, Vascular Cell Adhesion Molecule-1, respiratory system, Allergens, Flow Cytometry, Article, respiratory tract diseases, Eosinophils, Mice, Inbred C57BL, Mice, Airway Remodeling, Animals, Female, Leukocyte Rolling, Interleukin-5, Bronchoalveolar Lavage Fluid, Lung
Abstract

The role played by the beta-galactoside-binding lectin galectin-3 (Gal-3) in airway remodeling, a characteristic feature of asthma that leads to airway dysfunction and poor clinical outcome in humans, was investigated in a murine model of chronic allergic airway inflammation. Wild-type (WT) and Gal-3 knockout (KO) mice were subjected to repetitive allergen challenge with OVA up to 12 wk, and bronchoalveolar lavage fluid (BALF) and lung tissue collected after the last challenge were evaluated for cellular features associated with airway remodeling. Compared to WT mice, chronic OVA challenge in Gal-3 KO mice resulted in diminished remodeling of the airways with significantly reduced mucus secretion, subepithelial fibrosis, smooth muscle thickness, and peribronchial angiogenesis. The higher degree of airway remodeling in WT mice was associated with higher Gal-3 expression in the BALF as well as lung tissue. Cell counts in BALF and lung immunohistology demonstrated that eosinophil infiltration in OVA-challenged Gal-3 KO mice was significantly reduced compared with that WT mice. Evaluation of cellular mediators associated with eosinophil recruitment and airway remodeling revealed that levels of eotaxin-1, IL-5, IL-13, found in inflammatory zone 1, and TGF-beta were substantially lower in Gal-3 KO mice. Finally, leukocytes from Gal-3 KO mice demonstrated decreased trafficking (rolling) on vascular endothelial adhesion molecules compared with that of WT cells. Overall, these studies demonstrate that Gal-3 is an important lectin that promotes airway remodeling via airway recruitment of inflammatory cells, specifically eosinophils, and the development of a Th2 phenotype as well as increased expression of eosinophil-specific chemokines and profibrogenic and angiogenic mediators.

Published
2010

213. Galectin‐3 disruption impaired tumoral angiogenesis by reducing VEGF secretion from TGF β 1‐induced macrophages

Author

Machado, Camila Maria Longo, primary, Andrade, Luciana Nogueira Sousa, additional, Teixeira, Verônica Rodrigues, additional, Costa, Fabrício Falconi, additional, Melo, Camila Morais, additional, dos Santos, Sofia Nascimento, additional, Nonogaki, Suely, additional, Liu, Fu‐Tong, additional, Bernardes, Emerson Soares, additional, Camargo, Anamaria Aranha, additional, and Chammas, Roger, additional

Published
2014
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216. Galectin-12: A protein associated with lipid droplets that regulates lipid metabolism and energy balance.

Author

Yang, Ri-Yao, Yang, Ri-Yao, Havel, Peter J, Liu, Fu-Tong, Yang, Ri-Yao, Yang, Ri-Yao, Havel, Peter J, and Liu, Fu-Tong

Abstract

Galectin-12, a member of the galectin family of animal lectins, is preferentially expressed in adipocytes. We recently reported that this galectin is localized on lipid droplets, specialized organelles for fat storage. Galectin-12 regulates lipid degradation (lipolysis) by modulating lipolytic protein kinase A (PKA) signaling. Mice deficient in galectin-12 exhibit enhanced adipocyte lipolysis, increased mitochondria respiration, reduced adiposity and ameliorated insulin resistance associated with weight gain. The results suggest that galectin-12 may be a useful target for treatment of obesity-related metabolic conditions, such as insulin resistance, metabolic syndrome, and type 2 diabetes. Most previously described galectins largely reside in the cytosol, although they can also be induced to become associated with membrane-containing structures. Along with an in-depth characterization of galectin-12, this mini-review comments on this first report of a galectin normally localized specifically in an organelle that performs an important intracellular function. Further studies will help shed light on how this protein regulates cellular homeostasis, especially energy homeostasis, and provide additional insight into the intracellular functions of galectins.

Published
2012

217. Galectin-3 binds to CD45 on diffuse large B-cell lymphoma cells to regulate susceptibility to cell death.

Author

Clark, Mary C, Clark, Mary C, Pang, Mabel, Hsu, Daniel K, Liu, Fu-Tong, de Vos, Sven, Gascoyne, Randy D, Said, Jonathan, Baum, Linda G, Clark, Mary C, Clark, Mary C, Pang, Mabel, Hsu, Daniel K, Liu, Fu-Tong, de Vos, Sven, Gascoyne, Randy D, Said, Jonathan, and Baum, Linda G

Abstract

Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma and an aggressive malignancy. Galectin-3 (gal-3), the only antiapoptotic member of the galectin family, is overexpressed in DLBCL. While gal-3 can localize to intracellular sites, gal-3 is secreted by DLBCL cells and binds back to the cell surface in a carbohydrate-dependent manner. The major counterreceptor for gal-3 on DLBCL cells was identified as the transmembrane tyrosine phosphatase CD45. Removal of cell-surface gal-3 from CD45 with the polyvalent glycan inhibitor GCS-100 rendered DLBCL cells susceptible to chemotherapeutic agents. Binding of gal-3 to CD45 modulated tyrosine phosphatase activity; removal of endogenous cell-surface gal-3 from CD45 with GCS-100 increased phosphatase activity, while addition of exogenous gal-3 reduced phosphatase activity. Moreover, the increased susceptibility of DLBCL cells to chemotherapeutic agents after removal of gal-3 by GCS-100 required CD45 phosphatase activity. Gal-3 binding to a subset of highly glycosylated CD45 glycoforms was regulated by the C2GnT-1 glycosyltransferase, indicating that specific glycosylation of CD45 is important for regulation of gal-3-mediated signaling. These data identify a novel role for cell-surface gal-3 and CD45 in DLBCL survival and suggest novel therapeutic targets to sensitize DLBCL cells to death.

Published
2012

218. Galectin-3 regulates intracellular trafficking of EGFR through Alix and promotes keratinocyte migration.

Author

Liu, Wei, Liu, Wei, Hsu, Daniel K, Chen, Huan-Yuan, Yang, Ri-Yao, Carraway, Kermit L, Isseroff, Roslyn R, Liu, Fu-Tong, Liu, Wei, Liu, Wei, Hsu, Daniel K, Chen, Huan-Yuan, Yang, Ri-Yao, Carraway, Kermit L, Isseroff, Roslyn R, and Liu, Fu-Tong

Abstract

The EGFR-mediated signaling pathways are important in a variety of cellular processes, including cell migration and wound re-epithelialization. Intracellular trafficking of EGFR is critical for maintaining EGFR surface expression. Galectin-3, a member of an animal lectin family, has been implicated in a number of physiological and pathological processes. Through studies of galectin-3-deficient mice and cells isolated from these mice, we demonstrated that the absence of galectin-3 impairs keratinocyte migration and skin wound re-epithelialization. We have linked this pro-migratory function to a crucial role of cytosolic galectin-3 in controlling intracellular trafficking and cell surface expression of EGFR after EGF stimulation. Without galectin-3, the surface levels of EGFR are markedly reduced, and the receptor accumulates diffusely in the cytoplasm. This is associated with reduced rates of both endocytosis and recycling of the receptor. We have provided evidence that this previously unreported function of galectin-3 may be mediated through interaction with its binding partner Alix, which is a protein component of the ESCRT (endosomal sorting complex required for transport) machinery. Our results suggest that galectin-3 is potentially a critical regulator of a number of important cellular responses through its intracellular control of trafficking of cell surface receptors.

Published
2012

219. Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta.

Author

Ploix, Corinne, Ploix, Corinne, Zuberi, Riaz I, Liu, Fu-Tong, Carson, Monica J, Lo, David D, Ploix, Corinne, Ploix, Corinne, Zuberi, Riaz I, Liu, Fu-Tong, Carson, Monica J, and Lo, David D

Abstract

The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTbeta), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflammatory disease, CCL21/CCL19 and LTbeta have not been associated with the induction, recruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have examined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTbeta and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hyper-responsiveness in both knockout background recipients. Moreover, class II positive antigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTbeta.

Published
2009

221. Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+regulatory T cells and influences the course ofLeishmania majorinfection

Author

Fermino, Marise L., primary, Dias, Fabrício C., additional, Lopes, Carla D., additional, Souza, Maria A., additional, Cruz, Ângela K., additional, Liu, Fu-Tong, additional, Chammas, Roger, additional, Roque-Barreira, Maria Cristina, additional, Rabinovich, Gabriel A., additional, and Bernardes, Emerson S., additional

Published
2013
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223. Higher bone marrow LGALS3 expression is an independent unfavorable prognostic factor for overall survival in patients with acute myeloid leukemia

Author

Cheng, Chieh-Lung, primary, Hou, Hsin-An, additional, Lee, Ming-Cheng, additional, Liu, Chieh-Yu, additional, Jhuang, Jie-Yang, additional, Lai, Yan-Jun, additional, Lin, Chung-Wu, additional, Chen, Huan-Yuan, additional, Liu, Fu-Tong, additional, Chou, Wen-Chien, additional, Chen, Chien-Yuan, additional, Tang, Jih-Luh, additional, Yao, Ming, additional, Huang, Shang-Yi, additional, Ko, Bor-Sheng, additional, Wu, Shang-Ju, additional, Tsay, Woei, additional, and Tien, Hwei-Fang, additional

Published
2013
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226. Therapeutic effect of cytotoxic T lymphocyte antigen 4/immunoglobulin on a murine model of primary biliary cirrhosis

Author

Dhirapong, Amy, primary, Yang, Guo-Xiang, additional, Nadler, Steven, additional, Zhang, Weici, additional, Tsuneyama, Koichi, additional, Leung, Patrick, additional, Knechtle, Stuart, additional, Ansari, Aftab A., additional, Coppel, Ross L., additional, Liu, Fu-Tong, additional, He, Xiao-Song, additional, and Gershwin, M. Eric, additional

Published
2013
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228. Mast cells and immunological skin diseases.

Author

Navi, Daniel, Navi, Daniel, Saegusa, Jun, Liu, Fu-Tong, Navi, Daniel, Navi, Daniel, Saegusa, Jun, and Liu, Fu-Tong

Abstract

Mast cells play an important role in both adaptive and innate immunity, and a large body of literature demonstrates their functions in skin immunity. This article reviews the literature on the role of this cell type in the pathogenesis of a number of immunological skin diseases, including contact dermatitis, atopic dermatitis, immunobullous disease, scleroderma, and chronic graft-vs.-host disease. In all these diseases, mast cells are noted to increase in number and undergo degranulation in the affected skin, and in some cases, their specific mediators are detected. Elucidation of the contribution of mast cells to the pathogenesis of these diseases has been aided significantly by the use of animal models, especially mouse models. The studies of mast cell-deficient mice in conjunction with normal congenic mice have been particularly fruitful, although in some cases, such as contact dermatitis, a definitive conclusion has not been achieved despite extensive efforts. The role of mast cells in atopic dermatitis has also been suggested by studies of gene polymorphism, which have linked some of the mast cell-related genes to the disease. In the case of scleroderma and chronic graft-vs.-host disease, the function of mast cells in fibrosis is further supported by the ability of these cells and their mediators to induce activation and proliferation of fibroblasts. Therapies targeting mast cells may prove beneficial for treatment of these inflammatory and autoimmune diseases.

Published
2007

229. Glycolic Acid Silences Inflammasome Complex Genes, NLRC4 and ASC, by Inducing DNA Methylation in HaCaT Cells.

Author

Tang, Sheau-Chung, Yeh, Jih-I, Hung, Sung-Jen, Hsiao, Yu-Ping, Liu, Fu-Tong, and Yang, Jen-Hung

Subjects
HYDROXY acids, GLYCOLIC acid, INFLAMMASOMES, METHYLATION, POLYMERASE chain reaction
Abstract

AHAs (α-hydroxy acids), including glycolic acid (GA), have been widely used in cosmetic products and superficial chemical peels. Inflammasome complex has been shown to play critical roles in inflammatory pathways in human keratinocytes. However, the anti-inflammatory mechanism of GA is still unknown. The aim of this study is to investigate the relationship between the expression of the inflammasome complex and epigenetic modification to elucidate the molecular mechanism of the anti-inflammatory effect of GA in HaCaT cells. We evaluated NLRP3, NLRC4, AIM2, and ASC inflammasome complex gene expression on real-time polymerase chain reaction (PCR). Methylation changes were detected in these genes following treatment with DNA methyltransferase (DNMT) inhibitor 5-aza-2′-deoxycytidine (5-Aza) with or without the addition of GA using methylation-specific PCR (MSP). GA inhibited the expressions of these inflammasome complex genes, and the decreases in the expressions of mRNA were reversed by 5-Aza treatment. Methylation was detected in NLRC4 and ASC on MSP, but not in NLRP3 or AIM2. GA decreased NLRC4 and ASC gene expression by increasing not only DNA methyltransferase 3B (DNMT-3B) protein level, but also total DNMT activity. Furthermore, silencing of DNMT-3B (shDNMT-3B) increased the expressions of NLRC4 and ASC. Our data demonstrated that GA treatment induces hypermethylation of promoters of NLRC4 and ASC genes, which may subsequently lead to the hindering of the assembly of the inflammasome complex in HaCaT cells. These results highlight the anti-inflammatory potential of GA-containing cosmetic agents in human skin cells and demonstrate for the first time the role of aberrant hypermethylation in this process. [ABSTRACT FROM AUTHOR]

Published
2016
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230. Galectin-3 Regulates the Innate Immune Response of Human Monocytes

Author

Chung, Andrew W., primary, Sieling, Peter A., additional, Schenk, Mirjam, additional, Teles, Rosane M. B., additional, Krutzik, Stephan R., additional, Hsu, Daniel K., additional, Liu, Fu-Tong, additional, Sarno, Euzenir N., additional, Rea, Thomas H., additional, Stenger, Steffen, additional, Modlin, Robert L., additional, and Lee, Delphine J., additional

Published
2012
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234. Galectins: a family of animal beta-galactoside-binding lectins

Author

Barondes, Samuel H., Castronovo, Vincent, Cooper, Douglas N.W., Cummings, Richard D., Drickamer, Kurt, Feizi, Ten, Gitt, Michael A., Hirabayashi, Jun, Hughes, Colin, Kasai, Ken-ichi, Leffler, Hakon, Liu, Fu-Tong, Lotan, Reuben, Mercurio, Arthur M., Monsigny, Michel, Pillai, Shiv, Poirer, Francoise, Raz, Avraham, Rigby, Peter W.J., Rini, James M., and Wang, John L.

Subjects
Lectins -- Research, Carrier proteins -- Analysis, Cytosol -- Research, Biological sciences
Abstract

Galectins are a family of beta-galactoside-binding lectins with related amino acid sequences found in mammals. Galectins, found in the cytosol, do not have signal peptides, and isolate as soluble proteins. They are characterized by their affinity for beta-galactosides and sequence similarity at the carbohydrate-binding site.

Published
1994

240. Galectin-12

Author

Yang, Ri-Yao, primary, Havel, Peter, additional, and Liu, Fu-Tong, additional

Published
2012
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241. Contribution of spinal galectin-3 to acute herpetic allodynia in mice

Author

Takasaki, Ichiro, primary, Taniguchi, Kana, additional, Komatsu, Fumiaki, additional, Sasaki, Atsushi, additional, Andoh, Tsugunobu, additional, Nojima, Hiroshi, additional, Shiraki, Kimiyasu, additional, Hsu, Daniel K., additional, Liu, Fu-Tong, additional, Kato, Ichiro, additional, Hiraga, Koichi, additional, and Kuraishi, Yasushi, additional

Published
2012
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243. Galectin-3 modulates phagocytosis-induced stellate cell activation and liver fibrosis in vivo

Author

Jiang, Joy X., primary, Chen, Xiangling, additional, Hsu, Daniel K., additional, Baghy, Kornelia, additional, Serizawa, Nobuko, additional, Scott, Fiona, additional, Takada, Yoshikazu, additional, Takada, Yoko, additional, Fukada, Hiroo, additional, Chen, Jenny, additional, Devaraj, Sridevi, additional, Adamson, Roger, additional, Liu, Fu-Tong, additional, and Török, Natalie J., additional

Published
2012
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244. Protein Palmitoylation by ZDHHC13 Protects Skin against Microbial-Driven Dermatitis

Author

Chen, Li-Ying, Yang-Yen, Hsin-Fang, Tsai, Chun-Chou, Thio, Christina Li- Ping, Chuang, Hsiao-Li, Yang, Liang-Tung, Shen, Li-Fen, Song, I-Wen, Liu, Kai-Ming, Huang, Yen-Te, Liu, Fu-Tong, Chang, Ya-Jen, Chen, Yuan-Tsong, and Yen, Jeffrey J.Y.

Abstract

Atopic dermatitis is a complex chronic inflammatory skin disorder that results from intimate interactions among genetic predisposition, host environment, skin barrier defects, and immunological factors. However, a clear genetic roadmap leading to atopic dermatitis remains to be fully explored. From a genome-wide mutagenesis screen, deficiency of ZDHHC13, a palmitoylacyl transferase, has previously been associated with skin and multitissue inflammatory phenotypes. Here, we report that ZDHHC13 is required for skin barrier integrity and that deficiency of ZDHHC13 renders mice susceptible to environmental bacteria, resulting in persistent skin inflammation and an atopic dermatitis-like disease. This phenotype is ameliorated in a germ-free environment and is also attenuated by antibiotic treatment, but not by deletion of the Rag1 gene, suggesting that a microbial factor triggers inflammation rather than intrinsic adaptive immunity. Furthermore, skin from ZDHHC13-deficient mice has both elevated levels of IL-33 and type 2 innate lymphoid cells, reinforcing the role of innate immunity in the development of atopic dermatitis. In summary, our study suggests that loss of ZDHHC13 in skin impairs the integrity of multiple barrier functions and leads to a dermatitis lesion in response to microbial encounters.

Published
2017
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