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CEAおよびDPP-IV(CD26)の局在はタイト結合蛋白occludinに依存する(Localization of carcinoembryonic antigen (CEA) and dipeptidyl peptidase IV (CD26) depend on tight junction protein occludin)

徳永祐一, 小島隆, 飛岡弘敏, 村田雅樹, 高野賢一, 千葉英樹, 澤田典均

日本癌学会総会記事 ( (一社)日本癌学会 ) 64回 166 - 166 2005.09

ヒトアデノイド上皮における抗原提示細胞の分布とタイト結合の発現

小泉純一, 小島隆, 高野賢一, 黒瀬誠, 澤田典均, 氷見徹夫

口腔・咽頭科 ( 日本口腔・咽頭科学会 ) 18 ( 1 ) 167 - 167 2005.08

鼻科領域の炎症研究の新しい展開ヒト鼻粘膜におけるタイト結合による上皮バリアと抗原提示細胞

高野賢一, 小島隆, 澤田典均, 氷見徹夫

日本鼻科学会会誌 ( (一社)日本鼻科学会 ) 44 ( 3 ) 185 - 185 2005.08

マウス骨芽細胞におけるIGF-1によるタイト結合蛋白およびギャップ結合蛋白の変化

畠山尚子, 射場浩介, 小島隆, 高田潤一, 澤田典均, 山下敏彦

日本整形外科学会雑誌 ( (公社)日本整形外科学会 ) 79 ( 8 ) S784 - S784 2005.08

マウス骨芽細胞におけるIGF-1によるタイト結合蛋白およびギャップ結合蛋白の変化

畠山尚子, 射場浩介, 小島隆, 高田潤一, 澤田典均, 山下敏彦

日本骨代謝学会学術集会プログラム抄録集 ( (一社)日本骨代謝学会 ) 23回 270 - 270 2005.06

Knock down of Cx32 expression leads to alteration of claudins expression through activated MAP-kinase in primary cultures of rat hepatocytes

Takashi Kojima, Ken-ichi Takano, Masaki Murata, Masafumi Imamura, Hideki Chiba, Norimasa Sawada

CELL STRUCTURE AND FUNCTION ( JAPAN SOC CELL BIOLOGY ) 30 89 - 89 2005.06

Research paper, summary (international conference)

Localization of apical membrane markers carcinoembryonic antigen (CEA) and dipeptidyl peptidase IV (CD26) depend on the expression of tight junction protein occludin in a polarized human intestinal epithelial cell line T84

Yuichi Tokunaga, Takashi Kojima, Hirotoshi Tobioka, Masaki Murata, Ken-ichi Takano, Hideki Chiba, Norimasa Sawada

CELL STRUCTURE AND FUNCTION ( JAPAN SOC CELL BIOLOGY ) 30 88 - 88 2005.06

Research paper, summary (international conference)

p38 MAP-kinase regulates function of gap and tight junctions during regeneration of rat hepatocytes

T Yamamoto, T Kojima, M Murata, K Takano, M Go, N Hatakeyama, H Chiba, N Sawada

JOURNAL OF HEPATOLOGY ( ELSEVIER SCIENCE BV ) 42 ( 5 ) 707 - 718 2005.05

Background/Aims: Hepatocyte regeneration is considered to be associated with adaptive changes in expression of gap and tight junctions through multiple signal transduction pathways including p38 MAP-kinase. The role of the stress responsitive MAP-kinase, p38 MAP-kinase, signaling pathway in function of gap and tight junctions was examined during regeneration of rat hepatocytes in vivo and in vitro. Methods: We examined changes in formation, expression and function of gap and tight junctions in rat livers after 70% partial hepatectomy and in primary cultures of rat hepatocytes, by using a p38 MAP-kinase inhibitor, SB203580. Results: When p38 MAP-kinase was activated during partial hepatectomy, down-regulation of Cx32 and up-regulation of claudin-1 were observed. By SB203580 treatment, the down-regulation of Cx32 was inhibited and the up-regulation of claudin-1 was enhanced, well maintaining the structures of gap and tight junctions. SB203580 treatment did not affect the increase of hepatocyte proliferation. In EGF induced proliferative rat hepatocytes treated with SB203580, the expression and function of Cx32 and claudin-1 were increased. Conclusions: Dynamic changes of formation of gap and tight junctions during regeneration of rat hepatocytes in vivo and in vitro are in part controlled via a p38 MAP-kinase signaling pathway, and are independent of cell growth. © 2005 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

DOI

Glyceraldehyde-derived advanced glycation end-products preferentially induce VEGF expression and reduce GDNF expression in human astrocytes

H Miyajima, M Osanai, H Chiba, N Nishikiori, T Kojima, K Ohtsuka, N Sawada

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS ( ACADEMIC PRESS INC ELSEVIER SCIENCE ) 330 ( 2 ) 361 - 366 2005.05

The blood-brain barrier (BBB) is a biological unit composed of capillary endothelial cells and astrocytes. Here we examined the effects of various types of advanced glycation end-products (AGEs) on astrocytes and BBB-forming endothelial cells. While no type of AGE we examined changed the permeability of endothelial sheets, glyceraldehyde-derived AGE induced VEGF expression most significantly in astrocytes. The expression of glial cell line-derived neurotrophic factor (GDNF), which reduces the vascular permeability, was decreased in the astrocytes by treatment with glyceraldehyde-derived AGE. These results indicate that glyceraldehyde-derived AGE is the biologically active substance for astrocytes by regulating the VEGF and GDNF expression, which is causally contributing to an increase in the permeability of the BBB. (c) 2005 Elsevier Inc. All rights reserved.

DOI PubMed CiNii

HLA-DR- and CD11c-positive dendritic cells penetrate beyond well-developed epithelial tight junctions in human nasal mucosa of allergic rhinitis

K Takano, T Kojima, M Go, M Murata, S Ichimiya, T Himi, N Sawada

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY ( HISTOCHEMICAL SOC INC ) 53 ( 5 ) 611 - 619 2005.05

The epithelial barrier of the upper respiratory tract plays a crucial role in host defense. In this study, to elucidate whether there is antigen monitoring by dendritic cells (DCs) beyond the epithelial tight-junction barrier in allergic rhinitis, we investigated the expression and function of tight junctions and characterized DCs in the epithelium of nasal mucosa from patients with allergic rhinitis. In reverse transcription-polymerase chain reaction, mRNAs of tight-junction proteins occludin, JAM-1, ZO-1, and claudin-1, -4, -7, -8, -12, -13, and -14 were detected in the nasal mucosa. Occludin, JAM-1, and ZO-1 were colocalized in the uppermost layer in the pseudostratified epithelium of the nasal mucosa, whereas claudin-1, -4, and -7 were found throughout the epithelium. in freeze-fracture replicas of the nasal mucosa, continuous tight-junction strands formed well-developed networks. Epithelial barrier function measured by a dye tracer was well maintained in occludin-positive tight junctions in the epithelium of the nasal mucosa. HLA-DR- and CD11c-positive DCs expressed claudin-1 and penetrated beyond occludin in the epithelium of the nasal mucosa with, but not without, allergic rhinitis. These results indicate that DCs may easily access antigens beyond epithelial tight junctions in the human nasal mucosa of allergic rhinitis.

DOI

タイト結合蛋白occludinは生存シグナルの伝達に重要な役割を有する

村田雅樹, 小島隆, 高野賢一, 畠山尚子, 山本敏誠, 千葉英樹, 澤田典均

日本病理学会会誌 ( (一社)日本病理学会 ) 94 ( 1 ) 348 - 348 2005.03

骨芽細胞の分化過程におけるタイト結合蛋白の発現とその機能について

畠山尚子, 小島隆, 村田雅樹, 高野賢一, 千葉英樹, 澤田典均

日本病理学会会誌 ( (一社)日本病理学会 ) 94 ( 1 ) 277 - 277 2005.03

ヒトアデノイドにおける上皮内抗原提示細胞の分布と上皮タイト結合との関係

高野賢一, 小島隆, 郷充, 村田雅樹, 千葉英樹, 氷見徹夫, 澤田典均

日本病理学会会誌 ( (一社)日本病理学会 ) 94 ( 1 ) 376 - 376 2005.03

Activation of p21 (CIP1/WAF1) gene expression and inhibition of cell proliferation by overexpression of hepatocyte nuclear factor-4 alpha

H Chiba, T Itoh, S Satohisa, N Sakai, H Noguchi, M Osanai, T Kojima, N Sawada

EXPERIMENTAL CELL RESEARCH ( ELSEVIER INC ) 302 ( 1 ) 11 - 21 2005.01

The F9 murine embryonal carcinoma cell line provides an attractive system for studying epithelial differentiation and antiproliferative processes. We have recently established F9 cells expressing doxycycline-inducible hepatocyte nuclear factor (HNF)-4alpha and shown that HNF-4alpha triggers the gene expression of tight-junction molecules, occludin, claudin-6, and claudin-7, as well as formation of functional tight junctions and polarized epithelial morphology (Exp. Cell Res. 286, [2003] 288). Since these events were very similar to those induced by retinoids, we investigated whether HNF-4alpha, like retinoid receptors, was involved in the control of cell proliferation. We herein show that HNF-4alpha up-regulates expression of the p21 gene, but not the p15, p16, p18, p19, or p27 gene, in a p53-independent manner, and inhibits cell growth in F9 cells. Similar results were observed in rat lung endothelial cells, in which expression of HNF-4alpha is conditionally induced by doxycycline. Furthermore, we demonstrate, by reporter assay, that HNF-4alpha significantly elevates the transcriptional activity of the p21 promoter. Since, HNF-4alpha is expressed not only in the liver but also in organs containing epithelial cells, such as kidney, intestine, pancreas, and stomach, it might also play critical roles in the regulation of epithelial morphogenesis and proliferation in these organs. (C) 2004 Elsevier Inc, All rights reserved.

DOI PubMed CiNii

Expression and function of tight junctions in the crypt epithelium of human palatine tonsils

M Go, T Kojima, K Takano, M Murata, S Ichimiya, H Tsubota, T Himi, N Sawada

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY ( HISTOCHEMICAL SOC INC ) 52 ( 12 ) 1627 - 1638 2004.12

The human palatine tonsils have surface and crypt stratified epithelium and may be initiated via the epithelium to mount immune responses to various presenting antigens. Here we investigated the expression and function of tight junctions in the epithelium of human palatine tonsils from patients with tonsillar hypertrophy or recurrent tonsillitis. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, -7, -8, and -14 mRNAs were detected in tonsillar hypertrophy. Occludin and claudin-14 were expressed in the uppermost layer of the tonsil surface epithelium, whereas ZO-1, JAM-1, and claudin-1, -4, and -7 were found throughout the epithelium. In the crypt epithelium, claudin-4 was preferentially expressed in the upper layers. In freeze-fracture replicas, short fragments of continuous tight junction strands were observed but never formed networks. In the crypt epithelium of recurrent tonsillitis, the tracer was leaked from the surface regions where occludin and claudin-4 disappeared. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, and -14, but not claudin-7, mRNAs were decreased in recurrent tonsillitis compared with those of tonsillar hypertrophy. These studies suggest unique expression of tight junctions in human palatine tonsillar epithelium, and the crypt epithelium may possess an epithelial barrier different from that of the surface epithelium.

DOI

Oncogenic Raf-1 regulates epithelial to mesenchymal transition via distinct signal transduction pathways in an immortalized mouse hepatic cell line

MD Lan, T Kojima, M Osanai, H Chiba, N Sawada

CARCINOGENESIS ( OXFORD UNIV PRESS ) 25 ( 12 ) 2385 - 2395 2004.12

The epithelial to mesenchymal transition (EMT) is considered to be an important event during malignant tumor progression and metastasis. Although Raf/MEK/ERK signaling causes EMT, the mechanisms, including the signaling pathways, are as yet unclear. In the present study we have examined the effects of signal transduction pathways on oncogenic Raf-1-induced EMT, using an immortalized mouse hepatic cell line. Oncogenic Raf-1-induced EMT is characterized by down-regulation of adherens and tight junctions and the reorganization of actin. An active Raf-1 gene was introduced into a mouse hepatic cell line which was then treated with the MAP kinase inhibitor PD98059, the p38 MAP kinase inhibitor SB203580, the PI3 kinase inhibitor LY294002 or the c-Src tyrosine kinase inhibitor PP2. The expression and localization of the adherens and tight junction proteins E-cadherin, occludin, ZO-1, claudin-1 and claudin-2 were determined by western blotting, RT-PCR and immunocytochemistry. The barrier function of tight junctions was assessed by measurements of transepithelial electric resistance (TER) and permeability in terms of fluxes of [C-14]mannitol and [C-14]inulin. In Raf-1-transfected cells expression of occludin and claudin-2 was markedly down-regulated at the protein and mRNA levels and the TER value was decreased, while the permeability was increased. The distribution of ZO-1, pancadherin and F-actin was changed from linear to zipper-like structures at cell borders. In Raf-1-transfected cells treated with PD98059 and SB203580, but not LY294002, expression and localization of claudin-2, but not occludin, recovered, together with barrier function, measured as the TER value. The distributions of ZO-1, pancadherin and F-actin also recovered on treatment with PD98059 and SB203580, but not LY294002. Expression and localization of occludin recovered slightly on treatment with PP2. Thus, oncogenic Raf-1 regulates EMT via distinct MAP kinase, p38 MAP kinase and c-Src tyrosine kinase signal pathways in the mouse hepatic cell line.

DOI

IL-1 beta regulates expression of Cx32, occludin, and claudin-2 of rat hepatocytes via distinct signal transduction pathways

T Yamamoto, T Kojima, M Murata, K Takano, M Go, H Chiba, N Sawada

EXPERIMENTAL CELL RESEARCH ( ACADEMIC PRESS INC ELSEVIER SCIENCE ) 299 ( 2 ) 427 - 441 2004.10

The functions of gap and tight junctions are perturbed during the acute-phase response to liver injury. To elucidate the mechanism of proinflammatory cytokine IL-1beta responsible for regulation of hepatic gap and tight junctions, we analyzed expression and function of gap and tight junctions using a rat liver injury model and primary cultures of rat hepatocyte. In rat liver lobules at 24 h after thioacetamide (TAA) treatment, where some IL-1beta-positive non-parenchymal cells existed, disappearance of connexin32-positive spots at cell borders of the hepatocytes and increases of claudin-2 and occludin immunoreactivities in bile canalicular regions were observed. In primary cultures of rat hepatocytes, IL-1beta caused the disappearance of connexin32, which was reciprocal to the induction and localization of claudin-2 to cell membranes. The downregulated connexin32 expression was inhibited by treatment with a MAP-kinase inhibitor (PD98059), whereas the upregulated claudin-2 expression was blocked by p38 MAP and PI3-kinase inhibitors (SB203580 and LY294002). The changes of connexin32 and claudin-2 may be controlled at the transcriptional level via NF-kappaB, HNF-1alpha, and CDX2. Occludin was hyperphosphorylated by IL-1beta treatment and was inhibited by treatment with a PI3-kinase inhibitor. These results demonstrate that MAP-kinase, p38 MAP-kinase, and PI3-kinase are distinctly involved in the regulation of hepatic gap and tight junctions during the acute-phase response to IL-1beta. (C) 2004 Elsevier Inc. All rights reserved.

DOI PubMed CiNii

Connexin26 によるタイト結合機能の制御 : 難聴解析モデルとしてのヒト気管支上皮細胞株の応用

郷充, 小島隆, 高野賢一, 澤田典均, 氷見徹夫

Otology Japan 14 ( 4 ) 2004.09

CiNii

生体防御におけるヒト扁桃上皮のバリア機能の調節機構の解析

郷充, 小島隆, 高野賢一, 坪田大, 澤田典均, 氷見徹夫

口腔・咽頭科 = Stomato-pharyngology 17 ( 1 ) 2004.08

DOI CiNii

骨芽細胞の分化過程におけるタイト結合蛋白の発現とその機能について

畠山尚子, 射場浩介, 小島隆, 高田潤一, 澤田典均, 山下敏彦

日本整形外科学会雑誌 ( (公社)日本整形外科学会 ) 78 ( 8 ) S878 - S878 2004.08

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