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6篇 您的检索式:作者名="Tatsuki Itoh"
    题名 作者 年代 出处 被引量
1Increased Osteopontin-Positive Macrophage Expression in Colorectal Cancer Stroma with Synchronous Liver Metastasis显示文摘Motohiro Imano Kiyokata Okuno Tatsuki Itoh Eizaburo Ishimaru Takao Satou Hitoshi Shiozaki 2010World Journal of Surgery2010,,8:1
2Blockade of the Ras/MEK/ERK and Ras/PI3K/Akt pathways by statins reduces the expression of bFGF, HGF, and TGF-β as angiogenic factors in mouse osteosarcoma显示文摘Masanobu Tsubaki Yuzuru Yamazoe Masashi Yanae Takao Satou Tatsuki Itoh Junichi Kaneko Yasuhiro Kidera Kenzo Moriyama Shozo Nishida 2011Cytokine2011,,1:1
3Isolation of neural stem cells from damaged rat cerebral cortex after traumatic brain jnjury显示文摘Itoh Tatsuki fatatou 2005Neuroreport2005,16,15:1
4Increased apoptotic neuronal cell death and cognitive impairment at early phase after traumatic brain injury in aged rats显示文摘Tatsuki Itoh Motohiro Imano Shozo Nishida Masahiro Tsubaki Nobuyuki Mizuguchi Shigeo Hashimoto Akihiko Ito Takao Satou 2013Brain Structure and Function2013,,1:1
5A phase II trial of perioperative chemotherapy involving a single intraperitoneal administration of paclitaxel followed by sequential S‐1 plus intravenous paclitaxel for serosa‐positive gastric cancer显示文摘Ying‐Feng Peng Motohiro Imano Tatsuki Itoh Takao Satoh Yasutaka Chiba Haruhiko Imamoto Masahiro Tsubaki Shozo Nishida Takushi Yasuda Hiroshi Furukawa 2015J. Surg. Oncol2015,,8:1
6Epigallocatechin-3-gallate suppresses transforming growth factor-beta signaling by interacting with the transforming growth factor-beta typeⅡreceptor显示文摘AIM: To investigate the(-)-epigallocatechin-3-gallate(EGCG) binding to transforming growth factor-β(TGF-β) type Ⅱ receptor(TGFRⅡ).METHODS: The expression of α-smooth muscle actin(α-SMA) was used as a marker for fibrotic change inhuman lung fibroblast MRC-5 cells. The α-SMA expression level was determined by western blotting and immunohistological analysis. We examined whether the anti-fibrotic effects of EGCG on MRC-5 cells was dependent on antioxidant mechanism by using edaravone and N-acetylcysteine(NAC). The suppression effects of EGCG on Smad2/3 activation were studied by confocal fluorescence microscopy. The binding of EGCG to recombinant TGFRⅡ protein was analyzed by immunoprecipitation and affinity chromatography.RESULTS: When MRC-5 cells were treated with TGF-β, EGCG decreased the expression of α-SMA in a dose dependent manner, whereas catechin did not influence the α-SMA expression in the cells. Except for EGCG, antioxidant compounds(e.g., edaravone and NAC) had no effects on the TGF-β-induced α-SMA expression. Nuclear localization of phosphorylated Smad2/3 was observed after TGF-β treatment; however, EGCG treatment attenuated the nuclear transportation of Smad2/3 in the presence or absence of TGF-β. After a TGFRⅡ expression vector was introduced into COS-7 cells, cell lysates were untreated or treated with EGCG or catechin. The immunoprecipitation experiments using the lysates showed that EGCG dose-dependently bound to TGFRⅡ and that catechin did not at all. Affinity chromatography study indicated that EGCG would bind to TGFRⅡ.CONCLUSION: Our results demonstrate that EGCG interacts with TGFRⅡ and inhibits the expression of α-SMA via the TGF-β-Smad2/3 pathway in human lung fibroblast MRC-5 cells.Masaki Tabuchi Sumio Hayakawa Eiko Honda Kana Ooshima Tatsuki Itoh Koji Yoshida Ah-Mee Park Hideaki Higashino Mamoru Isemura Hiroshi Munakata 2013World Journal of Experimental Medicine2013,3,4:1
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