Details of a Researcher - Kosaka, Takeo

Papers - Kosaka, Takeo

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A case report of retroaortic left renal vein with tumor thrombus of renal cell carcinoma

Otsuki, Hideo, Kuroda, Kenji, Kosaka, Takeo, Ito, Keiichi, Hayakawa, Masamichi, Asano, Tomohiko

CLINICAL AND EXPERIMENTAL NEPHROLOGY 15 ( 3 ) 438 - 441 2011.06

Research paper (scientific journal), ISSN 1342-1751

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[History and current review of basic research for prostate cancer].

Kosaka Takeo, Oya Mototsugu

Nihon rinsho. Japanese journal of clinical medicine 69 Suppl 5 7 - 12 2011.06

ISSN 0047-1852

Hemodialysis case in which rcc was identified after disappearance of perirenal hematoma following spontaneous renal rupture treated by transcatheter arterial embolization

Otsuki Hideo, Ito Keiichi, Kosaka Takeo, Hamada Shinsuke, Takahashi Masahiro, Isono Makoto, Nakamura Kenzo, Kuwahara Yoshitaka, Kaji Tatsumi, Asano Tomohiko

Acta Urologica Japonica 57 ( 5 ) 247 - 250 2011.05

ISSN 0018-1994

A 55-year-old man who had been undergoing hemodialysis for 9 years visited our institution after the sudden onset of severe left flank pain. He presented with hypotension and was admitted immediately because computed tomography (CT) revealed a massive perirenal hematoma. Renal arteriography showed contrast media leakage at the lower branch of the left renal artery, and spontaneous renal rupture was diagnosed. Five months after the bleeding was stopped by selective transcatheter embolization of the branch of renal artery, CT showed an enhanced mass at the upper pole of left kidney and renal cell carcinoma (RCC) was suspected. Radical nephrectomy was performed, the pathological diagnosis was clear cell carcinoma, and the man has not experienced recurrence within 36 months after the surgery. RCC did not appear to be the cause of the original hemorrhage because there was a small residual hematoma in the middle of the renal parenchyma that was separated from the RCC. In cases of spontaneous renal rupture, re-evaluation by imaging studies is mandatory after disappearance of perirenal hematoma because imaging studies at the time of the rupture sometimes do not reveal the cause of the hemorrhage.

Ataxia-telangiectasia mutated (ATM) deficiency decreases reprogramming efficiency and leads to genomic instability in iPS cells

Kinoshita Taisuke, Nagamatsu Go, Kosaka Takeo, Takubo Keiyo, Hotta Akitsu, Ellis James, Suda Toshio

Biochemical and Biophysical Research Communications 407 ( 2 ) 321 - 326 2011.04

ISSN 0006-291X

During cell division, one of the major features of somatic cell reprogramming by defined factors, cells are potentially exposed to DNA damage. Inactivation of the tumor suppressor gene p53 raised reprogramming efficiency but resulted in an increased number of abnormal chromosomes in established iPS cells. Ataxia-telangiectasia mutated (ATM), which is critical in the cellular response to DNA double-strand breaks, may also play an important role during reprogramming. To clarify the function of ATM in somatic cell reprogramming, we investigated reprogramming in ATM-deficient (ATM-KO) tail-tip fibroblasts (TTFs). Although reprogramming efficiency was greatly reduced in ATM-KO TTFs, ATM-KO iPS cells were successfully generated and showed the same proliferation activity as WT iPS cells. ATM-KO iPS cells had a gene expression profile similar to ES cells and WT iPS cells, and had the capacity to differentiate into all three germ layers. On the other hand, ATM-KO iPS cells accumulated abnormal genome structures upon continuous passages. Even with the abnormal karyotype, ATM-KO iPS cells retained pluripotent cell characteristics for at least 20 passages. These data indicate that ATM does participate in the reprogramming process, although its role is not essential.

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Angiotensin II type 1 receptor expression and microvessel density in human bladder cancer

Shirotake Suguru, Miyajima Akira, Kosaka Takeo, Tanaka Nobuyuki, Maeda Takahiro, Kikuchi Eiji, Oya Mototsugu

Urology 77 ( 4 ) 2011.04

ISSN 0090-4295

Objectives: To determine whether angiotensin II type 1 receptor (AT1R) expression and tumor angiogenesis in human bladder cancer (BCa) specimens acquired by transurethral resection (TUR). It has recently been reported that AT1R is expressed in several tumors and is involved in tumor angiogenesis. However, no study has investigated AT1R expression in association with angiogenesis in clinical specimens of bladder cancer. Methods: Surgical specimens were obtained from 108 patients who had undergone TUR for bladder cancer. All specimens were pathologically diagnosed as urothelial carcinoma. AT1R expression and microvessel density (MVD) were determined by immunostaining. The clinical and pathologic characteristics were retrospectively reviewed. Results: The MVD was greater in muscle-invasive BCa (MIBC; 29 cases, 34.4 ± 4.1/0.25 mm²) than in non-MIBC (NMIBC; 79 cases, 17.4 ± 1.1/0.25 mm², P < .0001). AT1R expression was greater in the MIBC (P = .0004) and high-grade (P = .0063) specimens than in the NMIBC and low-grade specimens. In addition, the greater expression of AT1R was significantly associated with MVD (P < .05). In NMIBC, the factors significantly affecting recurrence-free survival on univariate analysis were AT1R (P = .02), MVD (P < .0001), tumor multiplicity (P = .0007), and bacille Calmette-Guérin intravesical instillation after TUR (P = .0026). Multivariate analysis revealed that tumor multiplicity and no BCG intravesical instillation after TUR were independent predictors of 5-year recurrence-free survival, and AT1R and MVD were independent predictors of 1-year recurrence-free survival (P < .01). Conclusions: AT1R expression and MVD were related to early intravesical recurrence in NMIBC. The results suggest that AT1R could become a new molecular target and a prognostic factor for NMIBC.

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Angiotensin II Type 1 Receptor Expression and Microvessel Density in Human Bladder Cancer

Shirotake, Suguru, Miyajima, Akira, Kosaka, Takeo, Tanaka, Nobuyuki, Maeda, Takahiro, Kikuchi, Eiji, Oya, Mototsugu

UROLOGY 77 ( 4 ) 1443 - 1458 2011.04

Research paper (scientific journal), ISSN 0090-4295

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Ataxia-telangiectasia mutated (ATM) deficiency decreases reprogramming efficiency and leads to gnomic instability in iPS cells

Kinoshita, Taisuke, Nagamatsu, Go, Kosaka, Takeo, Takubo, Keiyo, Hotta, Akitsu, Ellis, James, Suda, Toshio

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 407 ( 2 ) 321 - 326 2011.04

Research paper (scientific journal), ISSN 0006-291X

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A germ cell-specific gene, Prmt5, works in somatic cell reprogramming

Nagamatsu Go, Kosaka Takeo, Kawasumi Miyuri, Kinoshita Taisuke, Takubo Keiyo, Akiyama Hideo, Sudo Tetsuo, Kobayashi Takashi, Oya Mototsugu, Suda Toshio

Journal of Biological Chemistry 286 ( 12 ) 10641 - 10648 2011.03

ISSN 0021-9258

Germ cells possess the unique ability to acquire totipotency during development in vivo as well as give rise to pluripotent stem cells under the appropriate conditions in vitro. Recent studies in which somatic cells were experimentally converted into pluripotent stem cells revealed that genes expressed in primordial germ cells (PGCs), such as Oct3/4, Sox2, and Lin28, are involved in this reprogramming. These findings suggest that PGCs may be useful for identifying factors that successfully and efficiently reprogram somatic cells into toti- and/or pluripotent stem cells. Here, we show that Blimp-1, Prdm14, and Prmt5, each of which is crucial forPGCdevelopment, have the potential to reprogram somatic cells into pluripotent stem cells. Among them, Prmt5 exhibited remarkable reprogramming of mouse embryonic fibroblasts into which Prmt5, Klf4, and Oct3/4 were introduced. The resulting cells exhibited pluripotent gene expression, teratoma formation, and germline transmission in chimeric mice, all of which were indistinguishable from those induced with embryonic stem cells. These data indicate that some of the factors that play essential roles in germ cell development are also active in somatic cell reprogramming.

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A Germ Cell-specific Gene, Prmt5, Works in Somatic Cell Reprogramming

Nagamatsu, Go, Kosaka, Takeo, Kawasumi, Miyuri, Kinoshita, Taisuke, Takubo, Keiyo, Akiyama, Hideo, Sudo, Tetsuo, Kobayashi, Takashi, Oya, Mototsugu, Suda, Toshio

JOURNAL OF BIOLOGICAL CHEMISTRY 286 ( 12 ) 10641 - 10648 2011.03

Research paper (scientific journal), ISSN 0021-9258

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Transumbilical laparo-endoscopic single site surgery for adrenal cortical adenoma inducing primary aldosteronism

Miyajima Akira, Maeda Takahiro, Hasegawa Masanori, Takeda Toshikazu, Ishida Masaru, Kosaka Takeo, Kikuchi Eiji, Nakagawa Ken, Oya Mototsugu

BMC Research Notes 4 2011

Background: We have started using laparo-endoscopic single-site surgery (LESS) in urologic surgery, although its use has not gained momentum due to its level of difficulty. We here report our initial experience with transumbilical LESS for adrenal cortical adenoma by using a single port with a multichannel cannula (SILS port) and bent laparoscopic instrumentation. Findings. A multichannel port (SILS port), bent laparoscopic instrument (Roticulator Endo Mini-Shears) and Opti4 laparoscopic electrodes were used in all cases. The intraperitoneal space was approached through the umbilicus. The SILS port was placed through a 2 cm incision at the inner edge of the umbilicus. A 5 mm flexible laparoscope was introduced to keep the laparoscope outside, and surgical specimens were extracted using an Endocatch bag. In addition, as a case control study, we compared perioperative data of LESS adrenalectomy (LESS-A) with that of conventional laparoscopic adrenalectomy (LA). We performed transumbilical LESS-A for adrenal cortical adenoma in 12 cases, beginning in December, 2009. All procedures were successfully completed, with only one incision through the umbilicus, and without conversion to a standard laparoscopic approach. Mean operative time for LESS-A was 121.2± 7.8 min, which was slightly longer than LA (110.2± 7.3 min). For right adrenal tumors, we used a miniport (2 mm port) in addition to a SILS port, and were able to successfully perform adrenalectomy "with no visible scaring". Tumor laterality and patient BMI did not affect surgical morbidity in these procedures. Moreover, there was no significant difference between LESS-A and LA in blood loss, analgesic requirement, hospital stay, and scar satisfaction. Conclusions: The transumbilical approach in LESS for adrenalectomy is safe and feasible and also improves cosmetic outcome compared with standard laparoscopic procedures. Improvements in surgical devices may aid the further development of this approach.

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Expression of snail in upper urinary tract urothelial carcinoma

Kosaka Takeo, Kikuchi Eiji, Mikami Shuji, Miyajima Akira, Shirotake Suguru, Ishida Masaru, Okada Yasunori, Oya Mototsugu

Clinical Cancer Research 16 ( 23 ) 5814 - 5823 2010.12

ISSN 1078-0432

Purpose: There are few molecular markers known to predict upper urinary tract urothelial carcinomas (UTUC) prognosis. Snail, which contributes to epithelial-mesenchymal transition (EMT), has been documented in cancer progression, but not clear yet in UTUC. We therefore addressed the expression and biological significance of Snail in UTUC. Experimental Design: To elucidate the biological significance of Snail in UTUC, we examined the immunohistochemical expression of snail in UTUC and analyzed its clinical significance in 150 patients with UTUC. Biological effects of Snail in EMT and invasion were evaluated by using small interfering RNA (siRNA) specific for Snail in urothelial carcinoma cell lines and the Matrigel invasion assay. Results: Nuclear Snail staining was very weak in superficial UTUC. In contrast, strong Snail staining was observed in many of the nucleus of invasive UTUC. Snail expression was significantly higher in the high tumor stage, high grade, and in tumors showing lymphovascular invasion (LVI). Multivariate Cox regression analysis revealed that elevated Snail expression was a significant and an independent prognostic predictor of recurrence-free survival and cancer-specific survival. Patients with positive LVI and high Snail expression showed the worse outcome. Targeting of Snail mRNA expression in UMUC-3 cells with Snail-specific siRNA downregulated the mRNA expression of Snail, Vimentin, MMP2, and MMP9. Furthermore, the cells with siRNA for Snail showed decreased invasion activity in comparison with the cells transfected with a nontargeting siRNA. Conclusion: Snail-induced EMT represents a clinically relevant mechanism of UTUC progression and an attractive target for the treatment of patients with UTUC.

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Expression of Snail in Upper Urinary Tract Urothelial Carcinoma: Prognostic Significance and Implications for Tumor Invasion

Kosaka, Takeo, Kikuchi, Eiji, Mikami, Shuji, Miyajima, Akira, Shirotake, Suguru, Ishida, Masaru, Okada, Yasunori, Oya, Mototsugu

CLINICAL CANCER RESEARCH 16 ( 23 ) 5814 - 5823 2010.12

Research paper (scientific journal), ISSN 1078-0432

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Cis-dichlorodiammineplatinum upregulates angiotensin II type 1 receptors through reactive oxygen species generation and enhances VEGF production in bladder cancer

Tanaka Nobuyuki, Miyajima Akira, Kosaka Takeo, Shirotake Suguru, Hasegawa Masanori, Kikuchi Eiji, Oya Mototsugu

Molecular Cancer Therapeutics 9 ( 11 ) 2982 - 2992 2010.11

ISSN 1535-7163

We previously reported that angiotensin II type 1 receptor (AT1R) antagonists enhanced the cytotoxity of cis-dichlorodiammineplatinum (CDDP) in a bladder cancer xenograft model. To elucidate the synergistic mechanism, we investigated whether reactive oxygen species (ROS) generation induced by CDDP may affect the regulation of AT1R expression. Five invasive human bladder cancer cell lines, T24, UMUC-3, 5637, KU-1, and KU-19-19, were used in the in vitro study. For the in vivo study, T24 cells were used. We also examined AT1R and vascular endothelial growth factor (VEGF) expression in human bladder cancer specimens that had been treated with CDDP-based chemotherapy. The in vitro study showed that AT1R expression was significantly upregulated by CDDP in T24, KU-1, and KU-19-19 cells. On the other hand, AT1R expression was not changed in UMUC-3 and 5637 cells. ROS generation was also significantly upregulated by CDDP in T24, KU-1, and KU-19-19 cells. The upregulation of AT1R expression induced by CDDP was significantly suppressed by scavenging free radicals. Angiotensin II induced VEGF production in CDDP-treated cells; however, the AT1R antagonist significantly inhibited the increase in VEGF. The in vivo study results also showed that CDDP treatment upregulated AT1R expression, resulting in increased VEGF. Clinical specimens from patients who underwent cystectomy after neoadjuvant CDDP-based chemotherapy showed significantly higher AT1R and VEGF expression than corresponding transurethral resection specimens. Our findings indicate that CDDP upregulates AT1R expression though ROS generation and enhances VEGF production. Therefore, AT1R blockade may be an effective strategy for bladder cancer in combination with CDDP-based chemotherapy.

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Cis-dichlorodiammineplatinum Upregulates Angiotensin II Type 1 Receptors through Reactive Oxygen Species Generation and Enhances VEGF Production in Bladder Cancer

Tanaka, Nobuyuki, Miyajima, Akira, Kosaka, Takeo, Shirotake, Suguru, Hasegawa, Masanori, Kikuchi, Eiji, Oya, Mototsugu

MOLECULAR CANCER THERAPEUTICS 9 ( 11 ) 2982 - 2992 2010.11

Research paper (scientific journal), ISSN 1535-7163

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Regulation of human dendritic cells by a novel specific nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin

Shinoda Kazunobu, Nakagawa Ken, Kosaka Takeo, Tanaka Nobuyuki, Maeda Takahiro, Kono Hidaka, Mizuno Ryuichi, Kikuchi Eiji, Miyajima Akira, Umezawa Kazuo, Oya Mototsugu

Human Immunology 71 ( 8 ) 763 - 770 2010.08

ISSN 0198-8859

Regulation of antigen-presenting cells (APC) is crucial in controlling allograft rejection. Dendritic cells (DC) are the most potent APC and must mature to present antigens to T-cell receptors. During DC maturation, nuclear factor-κB (NF-κB) is a key transcriptional factor. We synthesized dehydroxymethylepoxyquinomicin (DHMEQ), which specifically inhibits the final step of nuclear translocation of activated NF-κB proteins and examined its immunoregulatory effects on human monocyte-derived DC (Mo-DC). Regulatory Mo-DC were generated by pretreatment with DHMEQ before LPS stimulation, which were termed dl-DC. DHMEQ pretreatment (5 μg/ml) completely inhibited nuclear translocation of activated NF-κB. DHMEQ significantly inhibited DC production of κproinflammatory cytokines (IL-6, TNF-α, and IL-12 p70) in a dose-dependent manner. IL-12 was most potently inhibited. However, IL-10 production by dl-DC was only moderately affected by DHMEQ. Although CD40 and the expression of HLA-DR (HLA-DR) expression on dl-DC was downregulated, CD80 and CD86 expression was moderately upregulated. Induction of T helper 1 cell responses was efficiently impaired by dl-DC. This confirmed that DHMEQ-treated Mo-DC exhibited immunoregulatory effects. These findings suggest that DHMEQ has potential as an immunosuppressive drug for human immune cells.

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Regulation of human dendritic cells by a novel specific nuclear factor-kappa B inhibitor, dehydroxymethylepoxyquinomicin

Shinoda, Kazunobu, Nakagawa, Ken, Kosaka, Takeo, Tanaka, Nobuyuki, Maeda, Takahiro, Kono, Hidaka, Mizuno, Ryuichi, Kikuchi, Eiji, Miyajima, Akira, Umezawa, Kazuo, Oya, Mototsugu

HUMAN IMMUNOLOGY 71 ( 8 ) 763 - 770 2010.08

Research paper (scientific journal), ISSN 0198-8859

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Adrenocortical zonation in humans under normal and pathological conditions

Nishimoto Koshiro, Nakagawa Ken, Li Dan, Kosaka Takeo, Oya Mototsugu, Mikami Shuji, Shibata Hirotaka, Itoh Hiroshi, Mitani Fumiko, Yamazaki Takeshi, Ogishima Tadashi, Suematsu Makoto, Mukai Kuniaki

Journal of Clinical Endocrinology and Metabolism 95 ( 5 ) 2296 - 2305 2010.05

ISSN 0021-972X

Context: Aldosterone synthase (CYP11B2) and steroid 11β-hydroxylase (CYP11B1) catalyze the terminal steps for aldosterone and cortisol syntheses, respectively, thereby determining the functional differentiationofhumanadrenocortical cells. Little isknown, however, about how the cells expressing the enzymes are actually distributed in the adrenals under normal and pathological conditions. Objective: The objective of the study was to determine the localization of CYP11B2 and -B1 in human adrenal specimens by using developed antibodies capable of distinguishing the two enzymes from each other. Results: Under normal conditions, CYP11B2 was sporadically detected in the zona glomerulosa, whereas CYP11B1 was entirely detected in the zonae fasciculata-reticularis. Adrenocortical cells lacking both enzymes were observed in the outer cortical regions. In addition to conventional zonation, we found a variegated zonation consisting of a subcapsular cell cluster expressing CYP11B2, which we termed aldosterone-producing cell cluster,andaCYP11B1- expressing area. Aldosterone-producing adenomas differed in cell populations expressing CYP11B2 from one another, whereas CYP11B1-expressing and double-negative cells were also intermingled. Adenomas from patients with Cushing's syndrome expressed CYP11B1 entirely but not CYP11B2, resulting in atrophic nontumor glands. The nontumor portions of both types of adenomas bore frequently one or more aldosterone-producing cell clusters, which sustained CYP11B2 expression markedly under the conditions of the suppressed renin-angiotensin system. Conclusion: Immunohistochemistry of the human normal adrenal cortex for CYP11B2 and CYP11B1 revealed a variegated zonation with cell clusters constitutively expressing CYP11B2. This technique may provide a pathological confirmatory diagnosis of adrenocortical adenomas.

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Adrenocortical Zonation in Humans under Normal and Pathological Conditions

Nishimoto, Koshiro, Nakagawa, Ken, Li, Dan, Kosaka, Takeo, Oya, Mototsugu, Mikami, Shuji, Shibata, Hirotaka, Itoh, Hiroshi, Mitani, Fumiko, Yamazaki, Takeshi, Ogishima, Tadashi, Suematsu, Makoto, Mukai, Kuniaki

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM 95 ( 5 ) 2296 - 2305 2010.05

Research paper (scientific journal), ISSN 0021-972X

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Role of Pelvic Lymph Node Dissection in Lymph Node-Negative Patients with Invasive Bladder Cancer

Shirotake, Suguru, Kikuchi, Eiji, Matsumoto, Kazuhiro, Yazawa, Satoshi, Kosaka, Takeo, Miyajima, Akira, Nakagawa, Ken, Oya, Mototsugu

JAPANESE JOURNAL OF CLINICAL ONCOLOGY 40 ( 3 ) 247 - 251 2010.03

Research paper (scientific journal), ISSN 0368-2811

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Ets-1 and hypoxia inducible factor-1α inhibition by angiotensin II type-1 receptor blockade in hormone-refractory prostate cancer

Kosaka Takeo, Miyajima Akira, Shirotake Suguru, Kikuchi Eiji, Hasegawa Masanori, Mikami Shuji, Oya Mototsugu

Prostate 70 ( 2 ) 162 - 169 2010.02

ISSN 0270-4137

BACKGROUND. Accumulating evidences have suggested that the renin-angiotensin system (RAS) participates in the regulation of tumor angiogenesis. We previously demonstrated that hormone-refractory prostate cancer (HRPC) showed significantly higher angiotensin II (Ang II) type-1 receptor (AT1R) expression, and that the AT1R blocker (ARB) exerted protective effects by inhibiting angiogenesis. However, the downstream transcriptional factors induced by Ang II in prostate cancer cells have not been fully elucidated yet. METHODS. Three human prostate cancer cell lines: LNCap, C4-2 and C4-2AT6 were used and analyzed. C4-2AT6 cells were established by culture in androgen-ablated conditioned medium for 6 months. RESULTS. C4-2AT6 cells showed significantly higher AT1R expression, accompanied by higher HIF-1α and Ets-1 expression in the nucleus. In C4-2AT6 cells, VEGF production was significantly higher than in C4-2 cells and LNCaP cells. These results suggested that HRPC exhibited aggressive angiogenic properties, accompanied by up-regulated HIF-1α and Ets-1. Ang II stimulated VEGF production in C4-2 cells and C4-2AT6 cells but not in LNCaP cells. ARB significantly inhibited VEGF production. Western blot analysis demonstrated that AngII induced nuclear expression of HIF-1α and Ets-1 in C4-2 and C4-2AT6 cells, but not in LNCaP cells. ARB significantly inhibited HIF-1α and Ets-1 induction in C4-2 and C4-2AT6 cells. CONCLUSIONS. This study suggests that AT1R blockade may have a significant impact on HRPCthrough the inhibition of HIF-1α and Ets-1 and the resulting suppression of angiogenesis. Our results provide the molecular basis of the clinical benefit of ARB as an angiogenic inhibitor in HRPC.

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