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Your search keyword '"Matozaki, Takashi"' showing total 339 results
Start Over Author "Matozaki, Takashi" Publication Type Academic Journals
339 results on '"Matozaki, Takashi"'

2. THBS1-producing tumor-infiltrating monocyte-like cells contribute to immunosuppression and metastasis in colorectal cancer

Author

Omatsu, Mayuki, Nakanishi, Yuki, Iwane, Kosuke, Aoyama, Naoki, Duran, Angeles, Muta, Yu, Martinez-Ordoñez, Anxo, Han, Qixiu, Agatsuma, Nobukazu, Mizukoshi, Kenta, Kawai, Munenori, Yamakawa, Go, Namikawa, Mio, Hamada, Kensuke, Fukunaga, Yuichi, Utsumi, Takahiro, Sono, Makoto, Masuda, Tomonori, Hata, Akitaka, Araki, Osamu, Nagao, Munemasa, Yoshikawa, Takaaki, Ogawa, Satoshi, Hiramatsu, Yukiko, Tsuda, Motoyuki, Maruno, Takahisa, Kogame, Toshiaki, Kasashima, Hiroaki, Kakiuchi, Nobuyuki, Nakagawa, Masahiro M., Kawada, Kenji, Yashiro, Masakazu, Maeda, Kiyoshi, Saito, Yasuyuki, Matozaki, Takashi, Fukuda, Akihisa, Kabashima, Kenji, Obama, Kazutaka, Ogawa, Seishi, Sheibani, Nader, Diaz-Meco, Maria T., Moscat, Jorge, and Seno, Hiroshi

Published
2023
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5. Protein-tyrosine phosphatase Shp2 positively regulates macrophage oxidative burst.

Author

Li, Xing, Goodwin, Charles, Nabinger, Sarah, Richine, Briana, Yang, Zhenyun, Hanenberg, Helmut, Ohnishi, Hiroshi, Matozaki, Takashi, Feng, Gen-Sheng, and Chan, Rebecca

Subjects
Macrophage, NADPH Oxidase, Pattern Recognition Receptor (PRR), Phagocytosis, Tyrosine-Protein Phosphatase (Tyrosine Phosphatase), Animals, Blotting, Western, Cells, Cultured, Extracellular Signal-Regulated MAP Kinases, Female, Fluorescent Antibody Technique, Immunoprecipitation, Integrases, Lectins, C-Type, Macrophages, Male, Mice, Mice, Knockout, Phagocytosis, Phosphorylation, Protein Tyrosine Phosphatase, Non-Receptor Type 11, Proto-Oncogene Proteins c-akt, Reactive Oxygen Species, Respiratory Burst, Signal Transduction, Tyrosine
Abstract

Macrophages are vital to innate immunity and express pattern recognition receptors and integrins for the rapid detection of invading pathogens. Stimulation of Dectin-1 and complement receptor 3 (CR3) activates Erk- and Akt-dependent production of reactive oxygen species (ROS). Shp2, a protein-tyrosine phosphatase encoded by Ptpn11, promotes activation of Ras-Erk and PI3K-Akt and is crucial for hematopoietic cell function; however, no studies have examined Shp2 function in particulate-stimulated ROS production. Maximal Dectin-1-stimulated ROS production corresponded kinetically to maximal Shp2 and Erk phosphorylation. Bone marrow-derived macrophages (BMMs) from mice with a conditionally deleted allele of Ptpn11 (Shp2(flox/flox);Mx1Cre+) produced significantly lower ROS levels compared with control BMMs. Although YFP-tagged phosphatase dead Shp2-C463A was strongly recruited to the early phagosome, its expression inhibited Dectin-1- and CR3-stimulated phospho-Erk and ROS levels, placing Shp2 phosphatase function and Erk activation upstream of ROS production. Further, BMMs expressing gain of function Shp2-D61Y or Shp2-E76K and peritoneal exudate macrophages from Shp2D61Y/+;Mx1Cre+ mice produced significantly elevated levels of Dectin-1- and CR3-stimulated ROS, which was reduced by pharmacologic inhibition of Erk. SIRPα (signal regulatory protein α) is a myeloid inhibitory immunoreceptor that requires tyrosine phosphorylation to exert its inhibitory effect. YFP-Shp2C463A-expressing cells have elevated phospho-SIRPα levels and an increased Shp2-SIRPα interaction compared with YFP-WT Shp2-expressing cells. Collectively, these findings indicate that Shp2 phosphatase function positively regulates Dectin-1- and CR3-stimulated ROS production in macrophages by dephosphorylating and thus mitigating the inhibitory function of SIRPα and by promoting Erk activation.

Published
2015

6. Macrophages require Skap2 and Sirpα for integrin-stimulated cytoskeletal rearrangement

Author

Alenghat, Francis J, Baca, Quentin J, Rubin, Nooreen T, Pao, Lily I, Matozaki, Takashi, Lowell, Clifford A, Golan, David E, Neel, Benjamin G, and Swanson, Kenneth D

Subjects
Biochemistry and Cell Biology, Biological Sciences, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Actin Cytoskeleton, Animals, Bone Marrow Cells, Cattle, Chemotaxis, Cytoskeleton, HEK293 Cells, Humans, Integrins, Intracellular Signaling Peptides and Proteins, Macrophage Colony-Stimulating Factor, Macrophages, Mice, Models, Biological, Polymerization, Protein Structure, Tertiary, Receptors, Immunologic, Signal Transduction, Inflammation, Integrin, Macrophage, Migration, Medical and Health Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

Macrophages migrate to sites of insult during normal inflammatory responses. Integrins guide such migration, but the transmission of signals from integrins into the requisite cytoskeletal changes is poorly understood. We have discovered that the hematopoietic adaptor protein Skap2 is necessary for macrophage migration, chemotaxis, global actin reorganization and local actin reorganization upon integrin engagement. Binding of phosphatidylinositol [3,4,5]-triphosphate to the Skap2 pleckstrin-homology (PH) domain, which relieves its conformational auto-inhibition, is critical for this integrin-driven cytoskeletal response. Skap2 enables integrin-induced tyrosyl phosphorylation of Src-family kinases (SFKs), Adap, and Sirpα, establishing their roles as signaling partners in this process. Furthermore, macrophages lacking functional Sirpα unexpectedly have impaired local integrin-induced responses identical to those of Skap2(-/-) macrophages, and Skap2 requires Sirpα for its recruitment to engaged integrins and for coordinating downstream actin rearrangement. By revealing the positive-regulatory role of Sirpα in a Skap2-mediated mechanism connecting integrin engagement with cytoskeletal rearrangement, these data demonstrate that Sirpα is not exclusively immunoinhibitory, and illuminate previously unexplained observations implicating Skap2 and Sirpα in mouse models of inflammatory disease.

Published
2012

9. Bibliometric analysis of organoids in regenerative medicine-related research worldwide over two decades (2002–2022).

Author

Setiawan, Jajar, Rizal, Dicky Moch, Sofyantoro, Fajar, Priyono, Dwi Sendi, Septriani, Nur Indah, Mafiroh, Wulan Usfi, Kotani, Takenori, Matozaki, Takashi, and Putri, Wahyu Aristyaning

Abstract

Aim: This study aimed to evaluate the trends in organoid culture research within the field of regenerative medicine from 2002 to 2022. Methods: The worldwide distribution of organoid research in regenerative medicine articles indexed in the Scopus database was analyzed. Result: A total of 840 documents were analyzed, averaging 42 publications annually. The USA (n = 296) led in publications, followed by China (n = 127), Japan (n = 91) and the UK (n = 75). Since 2011, research has surged, particularly in China, which emerged as a prominent center. Conclusion: The findings highlight significant growth in organoid research, promising future organ transplantation. Research trends integrate tissue engineering, gene modification and induced pluripotent stem cell technologies, reflecting a move toward personalized medicine. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Protein tyrosine phosphatase SAP-1 protects against colitis through regulation of CEACAM20 in the intestinal epithelium

Author

Murata, Yoji, Kotani, Takenori, Supriatna, Yana, Kitamura, Yasuaki, Imada, Shinya, Kawahara, Kohichi, Nishio, Miki, Daniwijaya, Edwin Widyanto, Sadakata, Hisanobu, Kusakari, Shinya, Mori, Munemasa, Kanazawa, Yoshitake, Saito, Yasuyuki, Okawa, Katsuya, Takeda-Morishita, Mariko, Okazawa, Hideki, Ohnishi, Hiroshi, Azuma, Takeshi, Suzuki, Akira, and Matozaki, Takashi

Published
2015

12. LAT1 expression influences Paneth cell number and tumor development in ApcMin/+ mice.

Author

Sui, Yunlong, Hoshi, Namiko, Ohgaki, Ryuichi, Kong, Lingling, Yoshida, Ryutaro, Okamoto, Norihiro, Kinoshita, Masato, Miyazaki, Haruka, Ku, Yuna, Tokunaga, Eri, Ito, Yuki, Watanabe, Daisuke, Ooi, Makoto, Shinohara, Masakazu, Sasaki, Kengo, Zen, Yoh, Kotani, Takenori, Matozaki, Takashi, Tian, Zibin, and Kanai, Yoshikatsu

Subjects
INTESTINAL tumors, GENE expression, SMALL intestine, MICE, TUMOR growth, CELL proliferation
Abstract

Background: Amino acid transporters play an important role in supplying nutrition to cells and are associated with cell proliferation. L-type amino acid transporter 1 (LAT1) is highly expressed in many types of cancers and promotes tumor growth; however, how LAT1 affects tumor development is not fully understood. Methods: To investigate the role of LAT1 in intestinal tumorigenesis, mice carrying LAT1 floxed alleles that also expressed Cre recombinase from the promoter of gene encoding Villin were crossed to an ApcMin/+ background (LAT1fl/fl; vil-cre; ApcMin/+), which were subject to analysis; organoids derived from those mice were also analyzed. Results: This study showed that LAT1 was constitutively expressed in normal crypt base cells, and its conditional deletion in the intestinal epithelium resulted in fewer Paneth cells. LAT1 deletion reduced tumor size and number in the small intestine of ApcMin/+ mice. Organoids derived from LAT1-deleted ApcMin/+ intestinal crypts displayed fewer spherical organoids with reduced Wnt/β-catenin target gene expression, suggesting a low tumor-initiation capacity. Wnt3 expression was decreased in the absence of LAT1 in the intestinal epithelium, suggesting that loss of Paneth cells due to LAT1 deficiency reduced the risk of tumor initiation by decreasing Wnt3 production. Conclusions: LAT1 affects intestinal tumor development in a cell-extrinsic manner through reduced Wnt3 expression in Paneth cells. Our findings may partly explain how nutrient availability can affect the risk of tumor development in the intestines. [ABSTRACT FROM AUTHOR]

Published
2023
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13. Targeting of SIRPα as a potential therapy for Langerhans cell histiocytosis.

Author

Okamoto, Takeshi, Murata, Yoji, Hasegawa, Daiichiro, Yoshida, Makiko, Tanaka, Daisuke, Ueda, Takashi, Hazama, Daisuke, Oduori, Okechi S., Komori, Satomi, Takai, Tomoko, Saito, Yasuyuki, Kotani, Takenori, Kosaka, Yoshiyuki, Maniwa, Yoshimasa, and Matozaki, Takashi

Abstract

Langerhans cell histiocytosis (LCH) is a rare neoplastic disorder characterized by inflammatory lesions arising from the anomalous accumulation of pathogenic CD1a+CD207+ dendritic cells (DCs). SIRPα is a transmembrane protein highly expressed in myeloid cells such as DCs and macrophages. Here we show that SIRPα is a potential therapeutic target for LCH. We found that SIRPα is expressed in CD1a+ cells of human LCH lesions as well as in CD11c+ DCs in the spleen, liver, and lung of a mouse model of LCH (BRAFV600ECD11c mouse), in which an LCH‐associated active form of human BRAF is expressed in a manner dependent on the mouse Cd11c promoter. BRAFV600ECD11c mice manifested markedly increased numbers of CD4+ T cells, regulatory T cells, and macrophages as well as of CD11c+MHCII+ DCs in the spleen. Monotherapy with a mAb to SIRPα greatly reduced the percentage of CD11c+MHCII+ DCs in peripheral blood, LCH‐like lesion size in the liver, and the number of CD11c+MHCII+ DCs in the spleen of the mutant mice. Moreover, this mAb promoted macrophage‐mediated phagocytosis of CD11c+ DCs from BRAFV600ECD11c mice, whereas it had no effects on the viability or CCL19‐dependent migration of such CD11c+ DCs or on their expression of the chemokine genes Ccl5, Ccl20, Cxcl11, and Cxcl12. Our results thus suggest that anti‐SIRPα monotherapy is a promising approach to the treatment of LCH that is dependent in part on the promotion of the macrophage‐mediated killing of LCH cells. [ABSTRACT FROM AUTHOR]

Published
2023
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24. Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis

Author

Koga, Takako, Inui, Masanori, Inoue, Kazuya, Kim, Sunhwa, Suematsu, Ayako, Kobayashi, Eiji, Iwata, Toshio, Ohnishi, Hiroshi, Matozaki, Takashi, Kodama, Tatsuhiko, Taniguchi, Tadatsugu, Takayanagi, Hiroshi, and Takai, Toshiyuki

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Takako Koga [1, 2, 6]; Masanori Inui [3, 6]; Kazuya Inoue [3]; Sunhwa Kim [1]; Ayako Suematsu [1, 2]; Eiji Kobayashi [3]; Toshio Iwata [3]; Hiroshi Ohnishi [4]; Takashi [...]

Published
2004
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25. The Role of Type-2 Conventional Dendritic Cells in the Regulation of Tumor Immunity.

Author

Saito, Yasuyuki, Komori, Satomi, Kotani, Takenori, Murata, Yoji, and Matozaki, Takashi

Subjects
TUMOR prevention, DENDRITIC cells, IMMUNE checkpoint inhibitors, IMMUNITY, TUMORS, CANCER vaccines, IMMUNOTHERAPY, PHARMACODYNAMICS
Abstract

Simple Summary: Recent studies revealed that type-2 conventional dendritic cells (cDC2s) play an important role in antitumor immunity by promoting cytotoxic T-cell responses and helper T-cell differentiation. This review outlines the role of cDC2s in tumor immunity and summarizes the latest progress regarding their potential in cancer vaccination and cDC2-targeted cancer immunotherapy. Conventional dendritic cells (cDCs) orchestrate immune responses to cancer and comprise two major subsets: type-1 cDCs (cDC1s) and type-2 cDCs (cDC2s). Compared with cDC1s, which are dedicated to the activation of CD8+ T cells, cDC2s are ontogenically and functionally heterogeneous, with their main function being the presentation of exogenous antigens to CD4+ T cells for the initiation of T helper cell differentiation. cDC1s play an important role in tumor-specific immune responses through cross-presentation of tumor-derived antigens for the priming of CD8+ T cells, whereas little is known of the role of cDC2s in tumor immunity. Recent studies have indicated that human cDC2s can be divided into at least two subsets and have implicated these cells in both anti- and pro-tumoral immune responses. Furthermore, the efficacy of cDC2-based vaccines as well as cDC2-targeted therapeutics has been demonstrated in both mouse models and human patients. Here we summarize current knowledge about the role of cDC2s in tumor immunity and address whether these cells are beneficial in the context of antitumor immune responses. [ABSTRACT FROM AUTHOR]

Published
2022
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