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Your search keyword '"Tsukita, Sachiko"' showing total 330 results
Start Over Author "Tsukita, Sachiko" Publication Type Academic Journals
330 results on '"Tsukita, Sachiko"'

5. Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs

Author

Sato, Ko, Matsumoto, Ikumi, Suzuki, Koya, Tamura, Atsushi, Shiraishi, Aki, Kiyonari, Hiroshi, Kasamatsu, Jun, Yamamoto, Hideki, Miyasaka, Tomomitsu, Tanno, Daiki, Miyahara, Anna, Zong, Tong, Kagesawa, Takafumi, Oniyama, Akiho, Kawamura, Kotone, Kitai, Yuki, Umeki, Aya, Kanno, Emi, Tanno, Hiromasa, Ishii, Keiko, Tsukita, Sachiko, and Kawakami, Kazuyoshi

Published
2021
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6. Inactivation of paracellular cation-selective claudin-2 channels attenuates immune-mediated experimental colitis in mice

Author

Raju, Preeti, Shashikanth, Nitesh, Tsai, Pei-Yun, Pongkorpsakol, Pawin, Chanez-Paredes, Sandra, Steinhagen, Peter R., Kuo, Wei-Ting, Singh, Gurminder, Tsukita, Sachiko, and Turner, Jerrold R.

Subjects
Chronic diseases -- Analysis, Genetic engineering -- Analysis, Permeability -- Analysis, Medical research -- Analysis, T cells -- Analysis, Colitis -- Analysis, Health care industry, Harvard University. Harvard Medical School
Abstract

The tight junction protein claudin-2 is upregulated in disease. Although many studies have linked intestinal barrier loss to local and systemic disease, these have relied on macromolecular probes. In vitro analyses show, however, that these probes cannot be accommodated by size- and charge-selective claudin-2 channels. We sought to define the impact of claudin-2 channels on disease. Transgenic claudin-2 overexpression or IL-13-induced claudin-2 upregulation increased intestinal small cation permeability in vivo. IL-13 did not, however, affect permeability in claudin-2-knockout mice. Claudin-2 is therefore necessary and sufficient to effect size- and charge-selective permeability increases in vivo. In chronic disease, T cell transfer colitis severity was augmented or diminished in claudin-2-transgenic or -knockout mice, respectively. We translated the in vitro observation that casein kinase-2 (CK2) inhibition blocks claudin-2 channel function to prevent acute, IL-13-induced, claudin-2-mediated permeability increases in vivo. In chronic immune-mediated colitis, CK2 inhibition attenuated progression in claudin-2-sufficient, but not claudin-2-knockout, mice, i.e., the effect was claudin-2 dependent. Paracellular flux mediated by claudin-2 channels can therefore promote immune-mediated colitis progression. Although the mechanisms by which claudin-2 channels intensify disease remain to be defined, these data suggest that claudin-2 may be an accessible target in immune-mediated disorders, including inflammatory bowel disease., Introduction Barriers that define distinct tissue compartments and separate self from non-self are necessary for survival of multicellular organisms. In some organs, for example the integument and bladder, the barrier [...]

Published
2020
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27. Frequent Alterations of Driver Genes in Chromosome X and Their Clinical Relevance in Extranodal NK/T-Cell Lymphoma

Author

Ito, Yuta, Marouf, Amira, Kogure, Yasunori, Koya, Junji, Tabata, Mariko, Saito, Yuki, Shingaki, Sumito, Yuasa, Mitsuhiro, Yamaguchi, Kentaro, Bruneau, Julie, Vavasseur, Manon, Dussiot, Michaël, Andre, Isabelle, Joshi, Akshay, Lagresle-Peyrou, Chantal, Magerus, Aude, Chaubard, Sammara, Lavergne, David, Bachy, Emmanuel, Brunet, Erika, Fataccioli, Virginie, Brouzes, Chantal, Laurent, Camille, De Leval, Laurence, Traverse-Glehen, Alexandra, Bossard, Céline, Parrens, Marie, Meignin, Véronique, Philippe, Laure, Rossignol, Julien, Suarez, Felipe, Michot, Jean-Marie, Tournilhac, Olivier, Bole-Feysot, Christine, Nitschke, Patrick, Tesson, Bruno, Laurent, Cécile, Molina, Thierry Jo, Asnafi, Vahid, Tsukita, Sachiko, Izutsu, Koji, Miyoshi, Hiroaki, Sakata, Seiji, Dobashi, Akito, Takeuchi, Kengo, Ohshima, Koichi, Gaulard, Philippe, Jaccard, Arnaud, Ogawa, Seishi, Hermine, Olivier, Kataoka, Keisuke, and Couronne, Lucile

Published
2022
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32. Double mutation of claudin‐1 and claudin‐3 causes alopecia in infant mice.

Author

Suzuki, Koya, Yamaga, Kosuke, Tokumasu, Reitaro, Katsuno, Tatsuya, Tanaka, Hiroo, Chiba, Shuhei, Yagi, Takeshi, Katayama, Ichiro, Tamura, Atsushi, Murota, Hiroyuki, and Tsukita, Sachiko

Subjects
HAIR follicles, CLAUDINS, HAIR growth, SEBACEOUS glands, INFANTS, BALDNESS, NONSENSE mutation
Abstract

Hair follicles (HFs) undergo cyclic phases of growth, regression, and rest in association with hair shafts to maintain the hair coat. Nonsense mutations in the tight junction protein claudin (CLDN)‐1 cause hair loss in humans. Therefore, we evaluated the roles of CLDNs in hair retention. Among the 27 CLDN family members, CLDN1, CLDN3, CLDN4, CLDN6, and CLDN7 were expressed in the inner bulge layer, isthmus, and sebaceous gland of murine HFs. Hair phenotypes were observed in Cldn1 weaker knockdown and Cldn3‐knockout (Cldn1Δ/ΔCldn3−/−) mice. Although hair growth was normal, Cldn1Δ/ΔCldn3−/− mice showed striking hair loss in the first telogen. Simultaneous deficiencies in CLDN1 and CLDN3 caused abnormalities in telogen HFs, such as an aberrantly layered architecture of epithelial cell sheets in bulges with multiple cell layers, mislocalization of bulges adjacent to sebaceous glands, and dilated hair canals. Along with the telogen HF abnormalities, which shortened the hair retention period, there was an enhanced proliferation of the epithelium surrounding HFs in Cldn1Δ/ΔCldn3−/− mice, causing accelerated hair regrowth in adults. Our findings suggested that CLDN1 and CLDN3 may regulate hair retention in infant mice by maintaining the appropriate layered architecture of HFs, a deficiency of which can lead to alopecia. [ABSTRACT FROM AUTHOR]

Published
2023
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