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Your search keyword '"Takizawa, Hajime"' showing total 14 results
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14 results on '"Takizawa, Hajime"'

2. Bronchial epithelial cells produce CXCL1 in response to LPS and TNFα: A potential role in the pathogenesis of COPD

Author

Inui, Toshiya, primary, Watanabe, Masato, additional, Nakamoto, Keitaro, additional, Sada, Mitsuru, additional, Hirata, Aya, additional, Nakamura, Masuo, additional, Honda, Kojiro, additional, Ogawa, Yukari, additional, Takata, Saori, additional, Yokoyama, Takuma, additional, Saraya, Takeshi, additional, Kurai, Daisuke, additional, Wada, Hiroo, additional, Ishii, Haruyuki, additional, and Takizawa, Hajime, additional

Published
2018
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3. IL-17A synergistically stimulates TNF-α-induced IL-8 production in human airway epithelial cells: A potential role in amplifying airway inflammation

Author

Honda, Kojiro, primary, Wada, Hiroo, additional, Nakamura, Masuo, additional, Nakamoto, Keitaro, additional, Inui, Toshiya, additional, Sada, Mitsuru, additional, Koide, Takashi, additional, Takata, Saori, additional, Yokoyama, Takuma, additional, Saraya, Takeshi, additional, Kurai, Daisuke, additional, Ishii, Haruyuki, additional, Goto, Hajime, additional, and Takizawa, Hajime, additional

Published
2016
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4. Interleukin-10 modulates pulmonary neutrophilic inflammation induced by cigarette smoke exposure

Author

Higaki, Manabu, primary, Wada, Hiroo, additional, Mikura, Shinichiro, additional, Yasutake, Tetsuo, additional, Nakamura, Masuo, additional, Niikura, Mamoru, additional, Kobayashi, Fumie, additional, Kamma, Hiroshi, additional, Kamiya, Shigeru, additional, Ito, Kazuhiro, additional, Barnes, Peter J., additional, Goto, Hajime, additional, and Takizawa, Hajime, additional

Published
2015
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6. C-REACTIVE PROTEIN MODULATES HUMAN LUNG FIBROBLAST MIGRATION

Author

Kikuchi, Kazuhiko, primary, Kohyama, Tadashi, additional, Yamauchi, Yasuhiro, additional, Kato, Jun, additional, Takami, Kazutaka, additional, Okazaki, Hitoshi, additional, Desaki, Masashi, additional, Nagase, Takahide, additional, Rennard, Stephen I., additional, and Takizawa, Hajime, additional

Published
2009
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13. Histamine induces human lung fibroblast-mediated collagen gel contraction via histamine H1 receptor.

Author

Horie, Masafumi, Saito, Akira, Yamauchi, Yasuhiro, Mikami, Yu, Sakamoto, Makiko, Jo, Taisuke, Nakajima, Jun, Takizawa, Hajime, Nagase, Takahide, and Kohyama, Tadashi

Subjects
ASTHMA, FIBROBLASTS, PHENOTYPES, COLLAGEN, HISTAMINE
Abstract

Background: Airway remodeling is implicated in irreversible airflow limitation of refractory asthma, which includes increased smooth muscle mass and subepithelial fibrosis. Activated fibroblasts acquire contractile phenotype to participate in tissue contraction and structural alteration of extracellular matrices. Histamine is a potent mediator of allergic inflammation, substantially involved in asthmatic pathophysiology. Objective: We hypothesized that histamine might play a role in airway remodeling, and investigated its effect on fibroblast-mediated collagen gel contraction. Methods: Fibroblast-mediated collagen gel contraction was studied. Histamine's regulation of collagen gel contraction was characterized by using specific histamine-receptor antagonists, an IP3 receptor antagonist and a PKC inhibitor. Results: Histamine induced contraction of collagen gels embedded with human lung fibroblasts, in a time-dependent manner, and at the concentration more than 10−6 M, both in four primary cultured adult lung fibroblasts and three fetal lung fibroblast cell lines. This effect was attenuated by H1 receptor antagonist, whereas those for H2 to H4 receptors failed to show an inhibitory effect. Furthermore, IP3 receptor-mediated Ca2+ mobilization was implicated in histamine's action on collagen gel contraction. Conclusions: Our results suggest that histamine is involved in airway remodeling through its action on lung fibroblasts, and antihistamine drugs, especially H1 receptor antagonists, might be potentially beneficial for a subset of asthmatic patients. [ABSTRACT FROM AUTHOR]

Published
2014
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14. Tumor necrosis factor-alpha enhances both epithelial-mesenchymal transition and cell contraction induced in A549 human alveolar epithelial cells by transforming growth factor-beta1.

Author

Yamauchi Y, Kohyama T, Takizawa H, Kamitani S, Desaki M, Takami K, Kawasaki S, Kato J, and Nagase T

Subjects
Cell Line, Tumor, Epithelial Cells drug effects, Epithelial Cells pathology, Fibrosis etiology, Humans, Mesenchymal Stem Cells pathology, Adenocarcinoma, Bronchiolo-Alveolar pathology, Cell Dedifferentiation drug effects, Cell Shape drug effects, Transforming Growth Factor beta1 pharmacology, Tumor Necrosis Factor-alpha pharmacology
Abstract

Recently, epithelial-mesenchymal transition (EMT) has been reported to contribute to tissue fibrosis through enhanced transforming growth factor (TGF)-beta1 signaling. Tumor necrosis factor (TNF)-alpha has also been implicated in tissue fibrosis. Therefore, the authors investigated whether TNF-alpha affected TGF-beta1-induced EMT. Cultured alveolar epithelial cells (A549 cells) were stimulated with TGF-beta1 (5 ng/mL), with/without TNF-alpha (10 ng/mL). TGF-beta1 induced EMT of A549 cells, with loss of E-cadherin and acquisition of vimentin. Combination of TNF-alpha with TGF-beta1 enhanced EMT, causing morphological changes, while quantitative polymerase chain reaction (PCR) showed suppression of E-cadherin mRNA and expression of vimentin mRNA. In addition, the gel contraction method revealed that cells that had undergone EMT acquired cell contractility, which is a feature of mesenchymal cells. Stimulation with TGF-beta1 induced cell contraction, as did TNF-alpha. Moreover, costimulation with TGF-beta1 and TNF-alpha enhanced the cell contraction. Although IFN-gamma suppressed spontaneous cell contraction, it did not suppress cell contraction, which was induced by TGF-beta1. In conclusion, TNF-alpha enhances not only EMT but also cell contraction induced by TGF-beta1. EMT might contribute to tissue fibrosis through induction of cell contraction.

Published
2010
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