Current Affiliation Organization 【 display / non-display 】

Current Affiliation Organization 【 display / non-display 】

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Research Interests 【 display / non-display 】

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Published Papers 【 display / non-display 】

• Development of a Mouse Experimental System for the In Vivo Characterization of Bioengineered Adipose-Derived Stromal Cells.

  Ichise T, Ichise H, Shimizu Y

  Cells   13 ( 7 )   2024.03 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Gastrin-releasing peptide regulates fear learning under stressed conditions via activation of the amygdalostriatal transition area.

  Goto F, Kiyama Y, Ogawa I, Okuno H, Ichise T, Ichise H, Anai M, Kodama T, Yoshida N, Bito H, Manabe T

  Molecular psychiatry   27 ( 3 ) 1694 - 1703   2022.01 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• S1PR1 regulates the quiescence of lymphatic vessels by inhibiting laminar shear stress-dependent VEGF-C signaling.

  Geng X, Yanagida K, Akwii RG, Choi D, Chen L, Ho Y, Cha B, Mahamud MR, Berman de Ruiz K, Ichise H, Chen H, Wythe J, Mikelis CM, Hla T, Srinivasan RS

  JCI insight   5 ( 14 )   2020.07 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  During the growth of lymphatic vessels (lymphangiogenesis), lymphatic endothelial cells (LECs) at the growing front sprout by forming filopodia. Those tip cells are not exposed to circulating lymph, as they are not lumenized. In contrast, LECs that trail the growing front are exposed to shear stress, become quiescent, and remodel into stable vessels. The mechanisms that coordinate the opposed activities of lymphatic sprouting and maturation remain poorly understood. Here, we show that the canonical tip cell marker Delta-like 4 (DLL4) promotes sprouting lymphangiogenesis by enhancing VEGF-C/VEGF receptor 3 (VEGFR3) signaling. However, in lumenized lymphatic vessels, laminar shear stress (LSS) inhibits the expression of DLL4, as well as additional tip cell markers. Paradoxically, LSS also upregulates VEGF-C/VEGFR3 signaling in LECs, but sphingosine 1-phosphate receptor 1 (S1PR1) activity antagonizes LSS-mediated VEGF-C signaling to promote lymphatic vascular quiescence. Correspondingly, S1pr1 loss in LECs induced lymphatic vascular hypersprouting and hyperbranching, which could be rescued by reducing Vegfr3 gene dosage in vivo. In addition, S1PR1 regulates lymphatic vessel maturation by inhibiting RhoA activity to promote membrane localization of the tight junction molecule claudin-5. Our findings suggest a potentially new paradigm in which LSS induces quiescence and promotes the survival of LECs by downregulating DLL4 and enhancing VEGF-C signaling, respectively. S1PR1 dampens LSS/VEGF-C signaling, thereby preventing sprouting from quiescent lymphatic vessels. These results also highlight the distinct roles that S1PR1 and DLL4 play in LECs when compared with their known roles in the blood vasculature.

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• CBP/p300 antagonises EGFR-Ras-Erk signalling and suppresses increased Ras-Erk signalling-induced tumour formation in mice.

  Ichise T, Yoshida N, Ichise H

  The Journal of pathology ( Wiley )  249 ( 1 ) 39 - 51   2019.09 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Establishment of a tamoxifen-inducible Cre-driver mouse strain for widespread and temporal genetic modification in adult mice.

  Ichise H, Hori A, Shiozawa S, Kondo S, Kanegae Y, Saito I, Ichise T, Yoshida N

  Experimental animals   65 ( 3 ) 231 - 44   2016.07 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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Other Papers 【 display / non-display 】

Other Papers 【 display / non-display 】

• Guidelines and Recommendations for the Care and Use of Fish, Amphibians, and Reptiles in Research, Testing, and Education

    37   33 - 35   2021.10  [Refereed]