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Your search keyword '"Kajikawa, Masunori"' showing total 15 results
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15 results on '"Kajikawa, Masunori"'

1. FZD5 regulates cellular senescence in human mesenchymal stem/stromal cells

Author

Harada, Seiko, primary, Mabuchi, Yo, additional, Kohyama, Jun, additional, Shimojo, Daisuke, additional, Suzuki, Sadafumi, additional, Kawamura, Yoshimi, additional, Araki, Daisuke, additional, Suyama, Takashi, additional, Kajikawa, Masunori, additional, Akazawa, Chihiro, additional, Okano, Hideyuki, additional, and Matsuzaki, Yumi, additional

Published
2020
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5. FZD5 regulates cellular senescence in human mesenchymal stem/stromal cells.

Author

Harada, Seiko, Mabuchi, Yo, Kohyama, Jun, Shimojo, Daisuke, Suzuki, Sadafumi, Kawamura, Yoshimi, Araki, Daisuke, Suyama, Takashi, Kajikawa, Masunori, Akazawa, Chihiro, Okano, Hideyuki, and Matsuzaki, Yumi

Subjects
MESENCHYMAL stem cells, GENE expression, AGING, STROMAL cells, TRANSCRIPTION factors
Abstract

Human mesenchymal stem/stromal cells (hMSCs) have garnered enormous interest as a potential resource for cell‐based therapies. However, the molecular mechanisms regulating senescence in hMSCs remain unclear. To elucidate these mechanisms, we performed gene expression profiling to compare clonal immature MSCs exhibiting multipotency with less potent MSCs. We found that the transcription factor Frizzled 5 (FZD5) is expressed specifically in immature hMSCs. The FZD5 cell surface antigen was also highly expressed in the primary MSC fraction (LNGFR+THY‐1+) and cultured MSCs. Treatment of cells with the FZD5 ligand WNT5A promoted their proliferation. Upon FZD5 knockdown, hMSCs exhibited markedly attenuated proliferation and differentiation ability. The observed increase in the levels of senescence markers suggested that FZD5 knockdown promotes cellular senescence by regulating the noncanonical Wnt pathway. Conversely, FZD5 overexpression delayed cell cycle arrest during the continued culture of hMSCs. These results indicated that the intrinsic activation of FZD5 plays an essential role in negatively regulating senescence in hMSCs and suggested that controlling FZD5 signaling offers the potential to regulate hMSC quality and improve the efficacy of cell‐replacement therapies using hMSCs. [ABSTRACT FROM AUTHOR]

Published
2021
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6. FZD5regulates cellular senescence in human mesenchymal stem/stromal cells

Author

Harada, Seiko, Mabuchi, Yo, Kohyama, Jun, Shimojo, Daisuke, Suzuki, Sadafumi, Kawamura, Yoshimi, Araki, Daisuke, Suyama, Takashi, Kajikawa, Masunori, Akazawa, Chihiro, Okano, Hideyuki, and Matsuzaki, Yumi

Abstract

Human mesenchymal stem/stromal cells (hMSCs) have garnered enormous interest as a potential resource for cell‐based therapies. However, the molecular mechanisms regulating senescence in hMSCs remain unclear. To elucidate these mechanisms, we performed gene expression profiling to compare clonal immature MSCs exhibiting multipotency with less potent MSCs. We found that the transcription factor Frizzled 5 (FZD5) is expressed specifically in immature hMSCs. The FZD5 cell surface antigen was also highly expressed in the primary MSC fraction (LNGFR+THY‐1+) and cultured MSCs. Treatment of cells with the FZD5 ligand WNT5A promoted their proliferation. Upon FZD5knockdown, hMSCs exhibited markedly attenuated proliferation and differentiation ability. The observed increase in the levels of senescence markers suggested that FZD5knockdown promotes cellular senescence by regulating the noncanonical Wnt pathway. Conversely, FZD5overexpression delayed cell cycle arrest during the continued culture of hMSCs. These results indicated that the intrinsic activation of FZD5plays an essential role in negatively regulating senescence in hMSCs and suggested that controlling FZD5 signaling offers the potential to regulate hMSC quality and improve the efficacy of cell‐replacement therapies using hMSCs. Although mesenchymal stem/stromal cells (MSCs) are promising for cell therapy, long‐term culture leads to MSC senescence with reduced stem cell capacity. We showed that FZD5, which is specifically expressed in immature MSCs, can serve as a stemness indicator. Controlling FZD5 signaling may improve MSC quality and the outcomes of cell therapy.

Published
2021
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8. HMGB1, a pathogenic molecule that induces neurite degeneration via TLR4-MARCKS, is a potential therapeutic target for Alzheimer’s disease

Author

Fujita, Kyota, primary, Motoki, Kazumi, additional, Tagawa, Kazuhiko, additional, Chen, Xigui, additional, Hama, Hiroshi, additional, Nakajima, Kazuyuki, additional, Homma, Hidenori, additional, Tamura, Takuya, additional, Watanabe, Hirohisa, additional, Katsuno, Masahisa, additional, Matsumi, Chiemi, additional, Kajikawa, Masunori, additional, Saito, Takashi, additional, Saido, Takaomi, additional, Sobue, Gen, additional, Miyawaki, Atsushi, additional, and Okazawa, Hitoshi, additional

Published
2016
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12. Human CD300C Delivers an Fc Receptor-γ-dependent Activating Signal in Mast Cells and Monocytes and Differs from CD300A in Ligand Recognition

Author

Takahashi, Mariko, primary, Izawa, Kumi, additional, Kashiwakura, Jun-ichi, additional, Yamanishi, Yoshinori, additional, Enomoto, Yutaka, additional, Kaitani, Ayako, additional, Maehara, Akie, additional, Isobe, Masamichi, additional, Ito, Shinichi, additional, Matsukawa, Toshihiro, additional, Nakahara, Fumio, additional, Oki, Toshihiko, additional, Kajikawa, Masunori, additional, Ra, Chisei, additional, Okayama, Yoshimichi, additional, Kitamura, Toshio, additional, and Kitaura, Jiro, additional

Published
2013
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13. A Soluble Form of LMIR5/CD300b Amplifies Lipopolysaccharide-Induced Lethal Inflammation in Sepsis

Author

Yamanishi, Yoshinori, primary, Takahashi, Mariko, additional, Izawa, Kumi, additional, Isobe, Masamichi, additional, Ito, Shinichi, additional, Tsuchiya, Akiho, additional, Maehara, Akie, additional, Kaitani, Ayako, additional, Uchida, Tomoyuki, additional, Togami, Katsuhiro, additional, Enomoto, Yutaka, additional, Nakahara, Fumio, additional, Oki, Toshihiko, additional, Kajikawa, Masunori, additional, Kurihara, Hiroki, additional, Kitamura, Toshio, additional, and Kitaura, Jiro, additional

Published
2012
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14. Characterization of Leukocyte Mono-immunoglobulin-like Receptor 7 (LMIR7)/CLM-3 as an Activating Receptor

Author

Enomoto, Yutaka, primary, Yamanishi, Yoshinori, additional, Izawa, Kumi, additional, Kaitani, Ayako, additional, Takahashi, Mariko, additional, Maehara, Akie, additional, Oki, Toshihiko, additional, Takamatsu, Reiko, additional, Kajikawa, Masunori, additional, Takai, Toshiyuki, additional, Kitamura, Toshio, additional, and Kitaura, Jiro, additional

Published
2010
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15. Interaction between Mutant Ataxin-1 and PQBP-1 Affects Transcription and Cell Death

Author

Okazawa, Hitoshi, primary, Rich, Tina, additional, Chang, Alex, additional, Lin, Xi, additional, Waragai, Masaaki, additional, Kajikawa, Masunori, additional, Enokido, Yasushi, additional, Komuro, Akihiko, additional, Kato, Seishi, additional, Shibata, Masao, additional, Hatanaka, Hiroshi, additional, Mouradian, M.Maral, additional, Sudol, Marius, additional, and Kanazawa, Ichiro, additional

Published
2002
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