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13 results on '"Kondo, Kiyotaka"'

2. Group III secreted phospholipase A2‐driven lysophospholipid pathway protects against allergic asthma

Author

Hamu‐Tanoue, Asako, primary, Takagi, Koichi, additional, Taketomi, Yoshitaka, additional, Miki, Yoshimi, additional, Nishito, Yasumasa, additional, Kano, Kuniyuki, additional, Aoki, Junken, additional, Matsuyama, Takahiro, additional, Kondo, Kiyotaka, additional, Dotake, Yoichi, additional, Matsuyama, Hiromi, additional, Machida, Kentaro, additional, Murakami, Makoto, additional, and Inoue, Hiromasa, additional

Published
2024
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4. Identification of distinct N-glycosylation patterns on extracellular vesicles from small-cell and non–small-cell lung cancer cells

Author

Kondo, Kiyotaka, primary, Harada, Yoichiro, additional, Nakano, Miyako, additional, Suzuki, Takehiro, additional, Fukushige, Tomoko, additional, Hanzawa, Ken, additional, Yagi, Hirokazu, additional, Takagi, Koichi, additional, Mizuno, Keiko, additional, Miyamoto, Yasuhide, additional, Taniguchi, Naoyuki, additional, Kato, Koichi, additional, Kanekura, Takuro, additional, Dohmae, Naoshi, additional, Machida, Kentaro, additional, Maruyama, Ikuro, additional, and Inoue, Hiromasa, additional

Published
2022
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6. Glycometabolic Regulation of the Biogenesis of Small Extracellular Vesicles

Author

Harada, Yoichiro, primary, Nakajima, Kazuki, additional, Suzuki, Takehiro, additional, Fukushige, Tomoko, additional, Kondo, Kiyotaka, additional, Seino, Junichi, additional, Ohkawa, Yuki, additional, Suzuki, Tadashi, additional, Inoue, Hiromasa, additional, Kanekura, Takuro, additional, Dohmae, Naoshi, additional, Taniguchi, Naoyuki, additional, and Maruyama, Ikuro, additional

Published
2020
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8. Generation of the heterogeneity of extracellular vesicles by membrane organization and sorting machineries

Author

Harada, Yoichiro, primary, Suzuki, Takehiro, additional, Fukushige, Tomoko, additional, Kizuka, Yasuhiko, additional, Yagi, Hirokazu, additional, Yamamoto, Mika, additional, Kondo, Kiyotaka, additional, Inoue, Hiromasa, additional, Kato, Koichi, additional, Taniguchi, Naoyuki, additional, Kanekura, Takuro, additional, Dohmae, Naoshi, additional, and Maruyama, Ikuro, additional

Published
2019
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12. IL-13 enhances mesenchymal transition of pulmonary artery endothelial cells via down-regulation of miR-424/503 in vitro.

Author

Takagi, Koichi, Yamakuchi, Munekazu, Matsuyama, Takahiro, Kondo, Kiyotaka, Uchida, Akifumi, Misono, Shunsuke, Hashiguchi, Teruto, and Inoue, Hiromasa

Subjects
*MESENCHYMAL stem cells, *PULMONARY artery, *ENDOTHELIAL cells, *DOWNREGULATION, *CELLULAR control mechanisms, *LIFE expectancy, *CELL migration
Abstract

Pulmonary arterial hypertension (PAH) has a major effect on life expectancy with functional degeneracy of the lungs and right heart. Interleukin-13 (IL-13), one of the type 2 cytokines mainly associated with allergic diseases, has recently been reported to be associated with Schistosomiasis-associated PAH which shares pathological features with other forms of PAH, such as idiopathic PAH and connective tissue disease-associated PAH. But a direct pathological role of IL-13 in the development of PAH has not been explored. We examined the effects of recombinant human IL-13 on the function of primary human pulmonary artery endothelial cells (HPAECs) to examine how IL-13 influences exacerbation of PAH. IL-13 increased the expression of Rictor, which is a key molecule of mammalian target of rapamycin complex 2. Treatment of IL-13 induced HPAEC migration via Rictor. Rictor was directly regulated by both miR-424 and 503 (miR-424/503). Therefore, IL-13 increases Rictor level by regulating miR-424/503, causing the increase of HPAEC migration. Since enhancement of HPAEC migration in the lung is thought to be associated with PAH, these data suggest that IL-13 takes some roles in exacerbating PAH. [ABSTRACT FROM AUTHOR]

Published
2018
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13. Group III secreted phospholipase A 2 -driven lysophospholipid pathway protects against allergic asthma.

Author

Hamu-Tanoue A, Takagi K, Taketomi Y, Miki Y, Nishito Y, Kano K, Aoki J, Matsuyama T, Kondo K, Dotake Y, Matsuyama H, Machida K, Murakami M, and Inoue H

Subjects
Humans, Animals, Mice, Lysophospholipids, Cytokines, Asthma, Respiratory Hypersensitivity, Phospholipases A2, Secretory genetics, Eosinophilia
Abstract

Asthma is a chronic inflammatory disease of the airways characterized by recurrent episodes of airway obstruction, hyperresponsiveness, remodeling, and eosinophilia. Phospholipase A 2 s (PLA 2 s), which release fatty acids and lysophospholipids from membrane phospholipids, have been implicated in exacerbating asthma by generating pro-asthmatic lipid mediators, but an understanding of the association between individual PLA 2 subtypes and asthma is still incomplete. Here, we show that group III-secreted PLA 2 (sPLA 2 -III) plays an ameliorating, rather than aggravating, role in asthma pathology. In both mouse and human lungs, sPLA 2 -III was expressed in bronchial epithelial cells and decreased during the asthmatic response. In an ovalbumin (OVA)-induced asthma model, Pla2g3 -/- mice exhibited enhanced airway hyperresponsiveness, eosinophilia, OVA-specific IgE production, and type 2 cytokine expression as compared to Pla2g3 +/+ mice. Lipidomics analysis showed that the pulmonary levels of several lysophospholipids, including lysophosphatidylcholine, lysophosphatidylethanolamine, and lysophosphatidic acid (LPA), were decreased in OVA-challenged Pla2g3 -/- mice relative to Pla2g3 +/+ mice. LPA receptor 2 (LPA 2 ) agonists suppressed thymic stromal lymphopoietin (TSLP) expression in bronchial epithelial cells and reversed airway hyperresponsiveness and eosinophilia in Pla2g3 -/- mice, suggesting that sPLA 2 -III negatively regulates allergen-induced asthma at least by producing LPA. Thus, the activation of the sPLA 2 -III-LPA pathway may be a new therapeutic target for allergic asthma., (© 2024 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)

Published
2024
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