Faculty Profiles - akihide Tanimoto

Papers - akihide Tanimoto

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T Morishita, M Tsutsui, H Shimokawa, K Sabanai, H Tasaki, O Suda, S Nakata, A Tanimoto, KY Wang, Y Ueta, Y Sasaguri, Y Nakashima, N Yanagihara . Nephrogenic diabetes insipidus in mice lacking all nitric oxide synthase isoforms . PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA102 ( 30 ) 10616 - 10621 2005.7Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：NATL ACAD SCIENCES

Nitric oxide (NO) is produced in almost all tissues and organs, exerting a variety of biological actions under physiological and pathological conditions. NO is synthesized by three different isoforms of NO synthase (NOS), including neuronal, inducible, and endothelial NOSs. Because there are substantial compensatory interactions among the NOS isoforms, the ultimate roles of endogenous NO in our body still remain to be fully elucidated. Here, we have successfully developed mice in which all three NOS genes are completely deleted by crossbreeding singly NOS-/- mice. NOS expression and activities were totally absent in the triply NOS-/- mice before and after treatment with lipopolysaccharide. Although the triply NOS-/- mice were viable and appeared normal, their survival and fertility rates were markedly reduced as compared with the wild-type mice. Furthermore, these mice exhibited marked hypotonic polyuria, polydipsia, and renal unresponsiveness to an antidiuretic hormone, vasopressin, all of which are characteristics consistent with nephrogenic diabetes insipidus. In the kidney of the triply NOS-/- mice, vasopressin-induced cAMP production and membranous aquaporin-2 water channel expression were reduced associated with tubuloglomerular lesion formation. These results provide evidence that the NOS system plays a critical role in maintaining homeostasis, especially in the kidney.

DOI： 10.1073/pnas.0502236102

中村雄介, 澤田寿仁, 的場周一郎, 横山剛, 志田勝義, 谷本昭英 . 小腸capillary hemangiomaに対して腹腔鏡補助下切除術を施行した1例 . 外科67 ( 7 ) 851 - 855 2005.7

Publisher：(株)南江堂

56歳男性.患者は貧血および血便を主訴に,精査加療目的で著者らの施設へ入院となった.入院時,正球性色素性貧血を認め,下部消化管内視鏡にてBauhin弁から約20cm口側の回腸に隆起性病変を発見し,腹腔鏡補助下小腸部分切除術を施行した.病理組織学的にcapillary hemangiomaと診断され,術後は経過良好であった

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Y Sasaguri, KY Wang, A Tanimoto, M Tsutsui, H Ueno, Y Murata, Y Kohno, S Yamada, H Ohtsu . Role of histamine produced by bone marrow-derived vascular cells in pathogenesis of atherosclerosis . CIRCULATION RESEARCH96 ( 9 ) 974 - 981 2005.5Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

To clarify the role of histamine-producing cells and its origin in atherosclerosis, we investigated histidine decarboxylase (HDC; histamine-producing enzyme) expression in murine arteries with vascular injuries after the animal had received transplanted bone marrow (BM) from green fluorescent protein (GFP)-transgenic mice. The neointima in the ligated carotid arteries contained BM-derived HDC+ cells that expressed macrophage (Mac-3) or smooth muscle cell antigen (α-SMA). In contrast, the HDC+ BM-derived cells, which were positive for Mac-3, were mainly located in the adventitia in the cuff replacement model. In apolipoprotein E-knockout mice on a high cholesterol diet, BM-derived cells expressing Mac-3 in the atheromatous plaques were also positive for HDC. In comparison with wild-type mice, HDC-/- mice showed reduced neointimal thickening and a decreased intima-to-media ratio after ligation and cuff replacement. These results indicate that histamine produced from BM-derived progenitor cells, which could transdifferentiate into SMC- or macrophage-like cells, are important for the formation of neointima and atheromatous plaques.

DOI： 10.1161/01.RES.0000166325.00383.ed

Y Murata, A Tanimoto, KY Wang, M Tsutsui, Y Sasaguri, F De Corte, H Matsushita . Granulocyte macrophage-colony stimulating factor increases the expression of histamine and histamine receptors in monocytes/macrophages in relation to arteriosclerosis . ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY25 ( 2 ) 430 - 435 2005.2Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Objective - To study the effect of granulocyte macrophage - colony-stimulating factor (GM-CSF) on histamine metabolism in arteriosclerosis, the expression of histidine decarboxylase (HDC; histamine-producing enzyme), histamine receptors 1 and 2 (HH1R and HH2R), and GM-CSF was investigated in human and mouse arteriosclerotic carotid arteries. Furthermore, the molecular mechanisms of GM-CSF - induced HDC and HH1R expression in monocytic U937 cells were investigated.
Methods and Results - Immunohistochemistry showed that atherosclerotic human coronary and mouse ligated carotid arteries contained HDC-expressing macrophages. Gene expression of HDC, HH1R, HH2R, and GM-CSF was also detected in the lesions. In U937 cells, GM-CSF enhanced histamine secretion and gene expression of HDC and HH1R. A promoter assay showed that GM-CSF enhanced gene transcription of HDC and HH1R but not HH2R.
Conclusion - The present results indicate that HDC and HHR are expressed in arteriosclerotic lesion, and that GM-CSF induces HDC and HH1R expression in monocytes. Locally produced histamine might participate in atherogenesis by affecting the expression of atherosclerosis-related genes in monocytes and smooth muscle cells.

DOI： 10.1161/01.ATV.0000148705.13411.65

Shigeo Hara, Yutaka Yamaguchi, Shigeko Hara, Akihide Tanimoto, Kunihiko Seki, Hiroshi Matsushita, Shinji Tomikawa, Keihachiro Kuzuhara . Long-term course of post-transplant mesangial IgA deposition: Clinicopathologic study of nine cases . Clinical Transplantation, Supplement19 ( 14 ) 32 - 40 2005

We conducted the present study to elucidate the fate of post-transplant mesangial IgA deposit under the long-term observation. Out of a total of 45 cases with post-transplant mesangial IgA deposition, nine cases with more than 4 yr of follow-up term were enrolled in this study, and clinicopathologic characteristics were described. The study included three men and six women with a mean age of 34.2 yr. The average observation time from the detection of mesangial IgA deposition was 6.1 yr. Three cases were categorized as recurrent IgA nephropathy, while six cases were classified into latent mesangial IgA deposition. One case with hypertension developed end-stage renal disease. The significant improvement in microscopic hematuria was observed in one recurrent IgA nephropathy case. Microscopic findings included mild mesangial stalk thickening in all but one case. IgA deposition demonstrated a significant decrease in three latent mesangial IgA deposition cases. No apparent reduction in dense deposit quantity was observed on electron microscopy. There was no association between clinicopathologic findings and the regimen of anti-immunosuppressive agents. This study showed the improvement of the disease activity did occur in both recurrent IgA nephropathy and latent mesangial IgA deposition. Further investigation of latent mesangial IgA deposition may present the important clue to the pathogenesis of IgA nephropathy. Copyright © Blackwell Munksgaard 2005.

S Hara, Y Yamaguchi, S Hara, A Tanimoto, K Seki, H Matsushita, S Tomikawa, K Kuzuhara . Long-term course of post-transplant mesangial IgA deposition: clinicopathologic study of nine cases . CLINICAL TRANSPLANTATION19 32 - 40 2005

Publisher：WILEY-BLACKWELL

We conducted the present study to elucidate the fate of posttransplant mesangial IgA deposit under the long-term observation. Out of a total of 45 cases with post-transplant mesangial IgA deposition nine cases with more than 4 yr of follow-up term were enrolled in this study, and clinicopathologic characteristics were described. The study included three men and six women with a mean age of 34.2 yr. The average observation time from the detection of mesangial IgA deposition was 6.1 yr. Three cases were categorized as recurrent IgA nephropathy, while six cases were classified into latent mesangial IgA deposition. One case with hypertension developed end-stage renal disease. The significant improvement in microscopic hematuria was observed in one recurrent IgA nephropathy case. Microscopic findings included mild mesangial stalk thickening in all but one case. IgA deposition demonstrated a significant decrease in three latent mesangial IgA deposition cases. No apparent reduction in dense deposit quantity was observed on electron microscopy. There was no association between clinicopathologic findings and the regimen of anti-immunosuppressive agents. This study showed the improvement of the disease activity did occur in both recurrent IgA nephropathy and latent mesangial IgA deposition. Further investigation of latent mesangial IgA deposition may present the important clue to the pathogenesis of IgA nephropathy.

DOI： 10.1111/j.1399-0012.2005.00402.x

久保孝利, 能勢卓, 谷本昭英, 笹栗靖之, 森陽, 伊東晃 . ウサギ関節軟骨の細胞外マトリックスおよびマトリックスメタロプロテアーゼ産生におよぼす加齢の影響 . Connective Tissue36 ( 4 ) 197 - 205 2004.12

Publisher：日本結合組織学会

ウサギ関節軟骨細胞を用い軟骨マトリックス合成の指標としてプロテオグリカン生合成,また分解の指標としてマトリックスメタロプロテアーゼ(MMPs)産生におよぼす加齢の影響を軟骨組織の組織学的変化とともに検討した.加齢によりウサギ関節組織では軟骨細胞数の減少とともにマトリックス合成能の減少によるマトリックス維持能の低下を認めた.また,軟骨細胞への炎症性メディエーターであるIL-1結合能の増加が起こり,IL-1によるMMPs産生をはじめとするマトリックス分解系の亢進が誘発されやすくなることが示唆された.したがって,これらが総合的に加齢による変形性関節症をはじめとする関節疾患の発症頻度増大の原因となる可能性が示唆された

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Ono C, Ashida T, Sugiyama T, Fujii J, Homma S, Tanimoto A . [Rupture of a thoracic aortic aneurysm in a patient with hypertension, myocardial infarction, hyperlipidemia and operation for abdominal aortic aneurysm rupture after follow-up for 28 years]. . Nihon Ronen Igakkai Zasshi41 ( 6 ) 670 - 674 2004.11Reviewed

Language：Japanese Publishing type：Research paper (scientific journal)

A Japanese man who died at age 86 had been followed since the age of 58, when he presented with hypertension of 150/95 mmHg. The patient remained socially active until he died suddenly of a ruptured thoracic aortic aneurysm, although he experienced angina pectoris in August 1974, and myocardial infarction was identified on electrocardiography in October 1974. He underwent operation for rectal cancer in 1987, and an abdominal aortic aneurysm 38mm in diameter was identified at that time. The patient underwent an operation for rupture of the abdominal aortic aneurysm in 1991. A thoracic aneurysm of 40 mm diameter was identified in 1995, and this expanded to 53 mm by 1997. Autopsy revealed a thoracic aortic aneurysm in the arch (8 x 5 x 5 cm) and descending aorta (7 x 7 x 8 cm). A large volume (2,080 ml) of bloody pleural fluid was present

DOI： 10.3143/geriatrics.41.670

Takashi Kato, Yoshifumi Ubara, Naoki Sawa, Tetsuo Tagami, Hideyuki Katori, Fumi Takemoto, Akihide Tanimoto, Kenmei Takaichi . A case of rheumatoid arthritis exhibiting accelerating rheumatoid pleurisy during low-dose weekly methotrexate therapy . Modern Rheumatology14 ( 5 ) 414 - 418 2004.11Reviewed International journal

Language：English Publishing type：Research paper (scientific journal)

A 75-year-old Japanese man suffering from rheumatoid arthritis (RA) had received methotrexate (MTX) treatment for 9 years and developed bilateral pleural thickening with exudative pleural effusions despite remission of the polyarthritis. A diagnosis of rheumatoid pleurisy, made by exclusion, was supported by the elevated rheumatoid factor level of the pleural fluid. The pleurisy developed concomitantly with MTX-induced leukocytopenia, and discontinuation of the MTX treatment partially improved the CRP level. These findings indicate a causal relation between the rheumatoid pleurisy and MTX and suggest that MTX therapy may be ineffective in the treatment of rheumatoid pleurisy. Treatment with 10 mg of prednisolone and 100 mg of cyclosporine A daily resulted in rapid resolution of the pleurisy. Although MTX-induced rheumatoid pleurisy is a rare condition, MTX therapy should be considered carefully in RA patients with concomitant rheumatoid pleurisy. © Japan College of Rheumatology and Springer-Verlag Tokyo 2004.

DOI： 10.1007/s10165-004-0337-y

小野周子, 芦田映直, 杉山卓郎, 藤井潤, 本間栄, 谷本昭英 . 高血圧,陳旧性心筋梗塞,高脂血症で28年間経過観察中に腹部大動脈瘤破裂術後11年で胸部大動脈瘤破裂にて死亡した86歳男性の1剖検例 . 日本老年医学会雑誌41 ( 6 ) 670 - 674 2004.11

Publisher：(一社)日本老年医学会

58歳男(初診時).労作時胸痛を主訴とした.50歳時に高血圧を発症したが無治療であった.心電図でV1-2に陰性T波,V3にq波を認め,心筋梗塞と診断し,患者の希望でプロプラノロール,イソソルビド硝酸塩を投与し自宅療養となった.以後発作は無かった.71歳時に直腸癌手術を施行し人工肛門を造設した.腹部大動脈瘤径38mmを腹部エコーで認めたが,β遮断薬による血圧コントロールで対処した.75歳時に腹痛と腹部膨満感が出現し,イレウスにて緊急手術を行ったところ,空腸腸間膜内に血腫を認め,イレウスの先進部と考えた.血腫の原因として,腹部大動脈瘤切迫破裂が考えられ,降圧療法後,腹部大動脈瘤に対して人工血管Y字グラフト置換術を施行した.77歳時に高脂血症に対してプラバスタチンを,高血圧に対してマニジピンを開始した.79歳時にCTで胸部大動脈瘤径40mmを認め,83歳時に62mmまで増大したが,患者の希望で手術は行わず,降圧薬内服による治療を開始した.86歳時に腹部大動脈瘤破裂で死亡した

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Y Kohno, A Tanimoto, C Cirathaworn, S Shimajiri, A Tawara, Y Sasaguri . GM-CSF activates RhoA, integrin and MMP expression in human monocytic cells . PATHOLOGY INTERNATIONAL54 ( 9 ) 693 - 702 2004.9Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

Monocyte migration is one of the key events occurring in the early stage of atherosclerosis. This process includes monocytic adhesion to and penetration through the arterial intima. In such an environment, many factors stimulate the monocytes to enhance integrin activation and extracellular matrix degradation. To investigate the coordinative operation of these two events in relation to monocyte migration, we paid particular attention to the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on monocytes in terms of RhoA activation and matrix metalloproteinase (MMP) expression. RhoA and integrin clustering were activated by GM-CSF, monocyte chemoattractant protein-1 (MCP-1) and platelet-derived growth factor-BB (PDGF-BB) in human monocytic cell lines. Furthermore, enhancement of migration was observed with stimulation by MCP-1 and PDGF-BB. Granulocyte-macrophage colony-stimulating factor did not enhance the migration, even though it activated RhoA and integrin. However, GM-CSF is known to stimulate monocytes to express MCP-1, suggesting the presence of an indirect mechanism for GM-CSF-mediated migratory activity. In contrast, only GM-CSF enhanced the expression of MMP-1 and MMP-9. These results provide evidence that GM-CSF has multiple functions enhancing monocytic migration via RhoA and integrin activation, and via MMP expression.

DOI： 10.1111/j.1440-1827.2004.01682.x

奥田逸子, 星原芳雄, 宇田川晴司, 小久保守, 谷本昭英 . 【Barrett食道癌表在癌の境界・深達度診断】Barrett食道癌の境界を読む範囲と深達度 X線の立場から . 胃と腸39 ( 9 ) 1223 - 1232 2004.8

S Kimura, KY Wang, A Tanimoto, Y Murata, Y Nakashima, Y Sasaguri . Acute inflammatory reactions caused by histamine via monocytes/macrophages chronically participate in the initiation and progression of atherosclerosis . PATHOLOGY INTERNATIONAL54 ( 7 ) 465 - 474 2004.7Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

Previously we demonstrated that histidine decarboxylase (HDC), which produces histamine from L-histidine, was detected in monocytes/macrophages located in human atherosclerotic lesions. As monocytic migration is a key event of atherogenesis, we investigated whether histamine induces monocytic expression of monocyte chemoattractant protein (MCP)-1 and its receptors CCR2-A and -B, and also endothelial expression of ICAM-1 and VCAM-1. Furthermore, we studied the effect of interleukin (IL)-4, which inhibits the HDC expression, on the expression of MCP-1 and CCR2. Histamine stimulated monocytes, but not macrophages, to express MCP-1 and CCR2-A and -B. The expression of MCP-1 was inhibited by histamine H2 blocker. In contrast, IL-4 enhanced CCR2 expression but not MCP-1. Histamine stimulated endothelial cells to express ICAM-1 and VCAM-1. These results indicate that histamine and IL-4, which are both synthesized in the arterial intima, chronically participates in the pathogenesis of atherosclerosis via the enhanced expression of monocytic MCP-1, CCR2 and endothelial adhesion molecules.

A Tanimoto, Y Matsuki, T Tomita, T Sasaguri, S Shimajiri, Y Sasaguri . Histidine decarboxylase expression in pancreatic endocrine cells and related tumors . PATHOLOGY INTERNATIONAL54 ( 6 ) 408 - 412 2004.6Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

Histidine decarboxylase (HDC) is an enzyme for decarboxylating L-histidine to histamine and is expressed in various types of cells including neuroendocrine tumors. Recent findings have demonstrated a high percentage of HDC immunoreactivity in many neuroendocrine tumors, including carcinoid tumors, small cell carcinomas of the lung, pheochromocytomas, and medullary carcinomas of the thyroid. HDC immunostaining was applied to pancreatic islet cells and related tumors to explore possible expression of HDC as a wide spectrum marker for neuroendocrine differentiation. A total of 24 cases (22 pancreatic endocrine neoplasms, one small cell carcinoma of the pancreas, and one mixed exocrine-endocrine carcinoma) along with normal pancreatic tissue were immunostained with the anti-HDC antibody. In a normal pancreas, a double immunostaining revealed possible colocalization of HDC with glucagon- or insulin-positive cells in the islets. Seventeen of 22 pancreatic endocrine neoplasms (77%) were found to be positive for HDC, and no distinct relation to hormonal activity was observed. One small cell carcinoma was strongly positive to HDC. One non-functional tumor with mixed exocrine and endocrine components showed a diffuse positive immunostaining for HDC, and some neoplastic glucagon- or somatostatin (SRIF)-positive cells coexpressed HDC. In conclusion, we demonstrated that the majority of pancreatic endocrine tumors expressed HDC, and we suggest that HDC is a wider new marker for neuroendocrine differentiation.

DOI： 10.1111/j.1440-1827.2004.01641.x

H Ikota, A Tanimoto, H Komatsu, Y Ozawa, H Matsushita . Ureteral leiomyoma causing hydronephrosis in Type 1 multiple endocrine neoplasia . PATHOLOGY INTERNATIONAL54 ( 6 ) 457 - 459 2004.6Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

A rare case of leiomyoma of the ureter in a patient with type 1 multiple endocrine neoplasia (MEN) is reported. The case is of a Japanese man in his forties who had a past history of parathyroid gland hyperplasia, pancreatic islet cell tumors, and bilateral adrenocortical nodular hyperplasia. The leiomyoma, measuring 15 x 13 x 12 mm, was located in the right upper ureter, obstructing the lumen and causing hydronephrosis. Three small leiomyomas were also detected in the lower portion. Furthermore, histological examination revealed three tiny leiomyomatous nodules embedded in the muscular layer. It has been reported that type 1 MEN is often complicated by multiple leiomyoma in many organs, including the esophagus, stomach, lung, uterus, and skin. However, it is believed that this is the first report of leiomyomatosis of the ureter occurring in a patient with type 1 MEN. It should be recognized that multiple ureteral leiomyomas may develop in patients of type 1 MEN and can potentially result in hydronephrosis. The multiple development of leiomyoma suggests a causal relationship to MEN1 gene alteration.

DOI： 10.1111/j.1440-1827.2004.01642.x

山本信彦, 星原芳雄, 志田勝義, 布袋屋修, 飯塚敏郎, 田中達朗, 橋本光代, 山本敬, 乳原善文, 谷本昭英 . 内視鏡的切除にて診断された回腸毛細血管腫の1例 . Gastroenterological Endoscopy46 ( 4 ) 949 - 954 2004.4

Publisher：(一社)日本消化器内視鏡学会

57歳女.ネフローゼ症候群と診断されており,腎不全にて血液透析が開始されていた.貧血に対してエリスロポエチン投与が行われたが徐々に進行し,当センター紹介入院となった.下部消化管内視鏡検査で回盲弁より10cmほど口側に径7mm大の隆起性病変があり,持続性に小量の出血が認められた.可動性があり内視鏡的切除可能と判断し,高周波ポリペクトミーを施行した.病理組織学的診断は毛細血管腫であった.切除後は貧血の改善がみられ,切除7ヵ月後に施行した内視鏡検査では,切除部位に瘢痕が認められるのみで,特に病変の遺残再発は認められなかった

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T Sasaguri, A Tanimoto, S Kimura, Y Kohno, M Hirasawa, Y Matsuki, K Abe, H Hashimoto, T Hamada, Y Sasaguri . Primary leiomyosarcoma of the vertebra: Case report and review of the literature . PATHOLOGY INTERNATIONAL54 ( 1 ) 73 - 76 2004.1Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

A case of primary leiomyosarcoma of a thoracic vertebra associated with a compression fracture in a 75-year-old woman was preoperatively thought to be granulation tissue. Surgical decompression was performed and the histological and immunohistochemical studies established the diagnosis of leiomyosarcoma. Based on the clinical and radiological examinations, metastases were ruled out. Primary leiomyosarcoma of the vertebra is extremely rare and in that site it is considered to have a relatively poor prognosis.

DOI： 10.1111/j.1440-1827.2004.01582.x

Sasaguri Y, Tanimoto A . Role of macrophage-derived histamine in atherosclerosis-- chronic participation in the inflammatory response --. . Journal of atherosclerosis and thrombosis11 ( 3 ) 122 - 130 2004Reviewed

Language：English Publishing type：Research paper (scientific journal)

The atherosclerotic intimal lesion contains endothelial cells, smooth muscle cells, monocytes/macrophages and T lymphocytes, which constitute a histamine-cytokine network that participates in chronic inflammatory responses. Monocytes/macrophages and T lymphocytes express the histamine-producing enzyme histidine decarboxylase (HDC), and specific histamine receptors (HHR), which are switched from HH2R to HHR1 during macrophage differentiation. Endothelial and smooth muscle cells also express HHR in response to histamine. The effects of histamine on these cells include a regulation of atherosclerosis-related events such as cell proliferation, expression of matrix metalloproteinase, adhesion molecules and cytokines. Furthermore, recent studies have indicated that histamine and the activation of its specific receptors modulate the Th1/Th2 balance in inflammatory lesions through the regulation of cytokine production from inflammatory cells. The histamine-cytokine network in the atherosclerotic intima could regulate inflammatory and immune responses, including Th1/Th2 balance, and contribute to atherogenesis.

DOI： 10.5551/jat.11.122

H Xu, A Tanimoto, Y Murata, S Kimura, KY Wang, Y Sasaguri . Difference in responsiveness of human esophageal squamous cell carcinoma lines to epidermal growth factor for MMP-7 expression . INTERNATIONAL JOURNAL OF ONCOLOGY23 ( 2 ) 469 - 476 2003.8Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：PROFESSOR D A SPANDIDOS

Expression of MMP-7 in human esophageal squamous cell carcinoma lines (TE-9 and -10) was investigated. Under normal culture conditions, immunocytochemical staining and enzymography demonstrated the production of MMP-7 in their cytoplasm and its gelatinolytic activity in the medium of TE-9 and -10 cell cultures. When EGF was added to the cultures, Western blotting, and RT-PCR analysis showed a dose-dependent increase in the amount of MMP-7 synthesized in the TE-9 cells, whereas in TE-10 cells, EGF failed to stimulate MMP-7 production. For luciferase reporter analysis of MMP-7 transcription, pMMP7LucWI (1132-bp) and pMMP7LucWII (334-bp) were cloned in the luciferase pGL3-basic vector. The promoter activity was enhanced from 1.5- to 2-fold by the addition of EGF to TE-9 cells transfected with pMMP7LucWI or WII, even though the response was low as compared with that of 12-O-tetradecanoyl-phorbol-13-acetate (TPA); and in TE-10 cells, only TPA enhanced the promoter activity of MMP-7. Luciferase promoter analysis using a pMMP7WII mutant series revealed that the AP-1 site was essential for transcription of the MMP-7 gene in TE-9 cells, and Tcf-I was also an important site, and that to a lesser degree, Tcf-II and PEA3s participated in the transcription of the MMP-7 gene in these cells. Unlike the results with TE-9 cells, in TE-10 cells, EGF failed to stimulate transcription of the MMP-7 gene; and up-regulation of the promoter activity by TPA was dependent on the AP-1 site and to lesser degree, on Tcf-I and Tcf-II. These results suggest that EGF plays also an important role in MMP-7 production of TE-9 cells and that there is a difference not only in EGF-intracellular signaling system but also in regulation mechanisms of MMP-7 transcription by beta-catenin-Tcf and/or PEA3 system between these 2 carcinoma lines.

K Aita, A Tanimoto, Y Fujimoto, S Momomura, F Takemoto, S Hara, H Matsushita . Sarcomatoid collecting duct carcinoma arising in the hemodialysis-associated acquired cystic kidney: An autopsy report . PATHOLOGY INTERNATIONAL53 ( 7 ) 463 - 467 2003.7Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

A case of sarcomatoid collecting duct carcinoma (CDC) arising in a long-term hemodialysis-associated acquired cystic kidney was reported. A 71-year-old woman with a 21-year history of hemodialysis showed a peritoneal metastatic carcinoma (carcinomatous peritonitis) with an unknown primary site. An autopsy revealed a sarcomatoid collecting duct carcinoma of the right kidney with multicyst formation. In addition to the carcinomatous peritonitis, the tumor metastasized to the lymph nodes and bilateral lung. The primary tumor was composed of both carcinomatous and sarcomatous components, suggesting a high-grade transformation. Carcinomatous tumor cells were positive for epithelial membranous antigen (EMA), cytokeratin, and reactive to soybean agglutinin and peanut agglutinin, whereas the sarcomatous cells were positive for vimentin as well as EMA. Thus, the immunohistochemical and lectin-histochemical analysis confirmed that the tumor originated in the medullary collecting duct. Although CDC is not common in acquired cystic kidney disease patients, attention should be given to the occurrence of high-grade carcinoma of rare histological variant, as well as conventional renal cell carcinoma.

DOI： 10.1046/j.1440-1827.2003.01502.x

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