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298 results on '"Isshiki, Keiji"'

6. Calorie restriction enhances cell adaptation to hypoxia through Sirt1-dependent mitochondrial autophagy in mouse aged kidney

Author

Kume, Shinji, Uzu, Takashi, Horiike, Kihachiro, Chin-Kanasaki, Masami, Isshiki, Keiji, Araki, Shin-ichi, Sugimoto, Toshiro, Haneda, Masakazu, Kashiwagi, Atsunori, and Koya, Daisuke

Subjects
Cell physiology -- Reorganization and restructuring -- Health aspects -- Physiological aspects -- Research, Autophagy (Cytology) -- Research -- Physiological aspects -- Health aspects, Kidneys -- Medical examination -- Research -- Physiological aspects -- Health aspects, Mitochondria -- Properties -- Research -- Physiological aspects -- Health aspects, Low-calorie diet -- Health aspects -- Research -- Physiological aspects, Hypoxia -- Physiological aspects -- Research, Company organization, Company restructuring/company reorganization, Health care industry
Abstract

Mitochondrial oxidative damage is a basic mechanism of aging, and multiple studies demonstrate that this process is attenuated by calorie restriction (CR). However, the molecular mechanism that underlies the beneficial effect of CR on mitochondrial dysfunction is unclear. Here, we investigated in mice the mechanisms underlying CR-mediated protection against hypoxia in aged kidney, with a special focus on the role of the NAD-dependent deacetylase sirtuin 1 (Sirt1), which is linked to CR-related longevity in model organisms, on mitochondrial autophagy. Adult-onset and long-term CR in mice promoted increased Sirt1 expression in aged kidney and attenuated hypoxia-associated mitochondrial and renal damage by enhancing BCL2/adenovirus E1B 19-kDa interacting protein 3-dependent (Bnip3-dependent) autophagy. Culture of primary renal proximal tubular cells (PTCs) in serum from CR mice promoted Sirt1-mediated forkhead box O3 (Foxo3) deacetylation. This activity was essential for expression of Bnip3 and p27Kip1 and for subsequent autophagy and cell survival of PTCs under hypoxia. Furthermore, the kidneys of aged [Sirt1.sup.±] mice were resistant to CR-mediated improvement in the accumulation of damaged mitochondria under hypoxia. These data highlight the role of the Sirt1-Foxo3 axis in cellular adaptation to hypoxia, delineate a molecular mechanism of the CR-mediated antiaging effect, and could potentially direct the design of new therapies for age- and hypoxia-related tissue damage., Introduction Increasing age causes progressive postmaturational deterioration of tissues and organs, leading to impairment of tissue functioning, increased vulnerability to challenges, and death. The kidney is a typical target organ [...]

Published
2010
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9. Structural and functional changes in the kidneys of high-fat diet-induced obese mice

Author

Deji, Naoko, Kume, Shinji, Araki, Shin-ichi, Soumura, Mariko, Sugimoto, Toshiro, Isshiki, Keiji, Chin-Kanasaki, Masami, Sakaguchi, Masayoshi, Koya, Daisuke, Haneda, Masakazu, Kashiwagi, Atsunori, and Uzu, Takashi

Subjects
Metabolic syndrome X -- Research, Metabolic syndrome X -- Health aspects, Kidney diseases -- Risk factors, Ketogenic diet -- Health aspects, Biological sciences
Abstract

Metabolic syndrome has been reported to be associated with chronic kidney disease, but the mechanisms remain unclear. Although feeding of a high-fat diet (HFD) to C57BL/6 mice is reported to induce systemic metabolic abnormalities and subsequent renal injuries, such as albuminuria, similar to human metabolic syndrome, alterations in HFD-induced renal injuries have not been fully elucidated in detail. We therefore investigated the structural and functional changes in the kidneys of C57BL/6 mice on a HFD. Six-week-old mice were fed a low-fat diet (LFD; 10% of total calories from fat) or a HFD (60% fat) for 12 wk. Mice fed a HFD showed significant increases in body weight, systolic blood pressure, plasma insulin, glucose, and triglycerides compared with those on a LFD. Accompanying these systemic changes, mice on a HFD showed albuminuria, an increase in glomerular tuft area, and mesangial expansion. These systemic and renal alterations in mice on a HFD were prevented by body weight control with the dietary restriction of feeding a HFD. Furthermore, mice on a HFD showed renal patho-physiological alterations including renal lipid accumulation, an increased accumulation of type IV collagen in glomeruli, an increase in macrophage infiltration in the renal medulla, an increase in urinary 8-hydroxy-2'-deoxyguanosine excretion, and impaired sodium handling. In conclusion, this study suggests that local metabolic alterations in the kidney play important roles in the development of renal injury associated with metabolic syndrome in addition to systemic metabolic changes and an increase in body weight. metabolic syndrome; dietary restriction; lipotoxicity; inflammation; salt-sensitive hypertension

Published
2009

13. Characterization of protein kinase C [beta] isoform's action on retinoblastoma protein phosphorylation, vascular endothelial growth factor-induced endothelial cell proliferation, and retinal neovascularization

Author

Suzuma, Kiyoshi, Takahara, Noriko, Suzuma, Izumi, Isshiki, Keiji, Ueki, Kohjiro, Leitges, Michael, Aiello, Lloyd Paul, and King, George L.

Subjects
Protein kinases -- Research, Cell proliferation -- Physiological aspects, Neovascularization -- Physiological aspects, Cellular signal transduction -- Physiological aspects, Vascular endothelial growth factor -- Physiological aspects, Science and technology
Abstract

Retinal neovascularization is a major cause of blindness and requires the activities of several signaling pathways and multiple cytokines. Activation of protein kinase C (PKC) enhances the angiogenic process and is involved in the signaling of vascular endothelial growth factor (VEGF). We have demonstrated a dramatic increase in the angiogenic response to oxygen-induced retinal ischemia in transgenic mice overexpressing PKC[beta]2 isoform and a significant decrease in retinal neovascularization in PKC[beta] isoform null mice. The mitogenic action of VEGF, a potent hypoxia-induced angiogenic factor, was increased by 2-fold in retinal endothelial cells by the overexpression of PKC[beta]1 or [beta]2 isoforms and inhibited significantly by the overexpression of a dominant-negative PKC[beta]2 isoform but not by the expression of PKC [alpha], [delta], and [zeta] isoforms. Association of PKC[beta]32 isoform with retinoblastoma protein was discovered in retinal endothelial cells, and PKC[beta]2 isoform increased retinoblastoma phosphorylation under basal and VEGF-stimulated conditions. The potential functional consequences of PKC[beta]-induced retinoblastoma phosphorylation could include enhanced E2 promoter binding factor transcriptional activity and increased VEGF-induced endothelial cell proliferation.

Published
2002

43. Overexpression of acetyl CoA carboxylase β exacerbates podocyte injury in the kidney of streptozotocin-induced diabetic mice

Author

Tanaka, Yuki, primary, Kume, Shinji, additional, Maeda, Shiro, additional, Osawa, Norihisa, additional, Takeda, Naoko, additional, Chin-Kanasaki, Masami, additional, Isshiki, Keiji, additional, Ugi, Satoshi, additional, Oshima, Itsuki, additional, Uzu, Takashi, additional, Maegawa, Hiroshi, additional, and Araki, Shin-ichi, additional

Published
2018
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45. Arterial stiffness and renal impairment in non‐proteinuric type 2 diabetic patients

Author

Nakao, Keiko, Uzu, Takashi, Araki, Shin‐ichi, Kume, Shinji, Deji, Naoko, Chin‐Kanasaki, Masami, Araki, Hisazumi, Isshiki, Keiji, Sugimoto, Toshiro, Kawai, Hiromichi, Nishio, Yoshihiko, Kashiwagi, Atsunori, and Maegawa, Hiroshi

Subjects
Clinical Science and Care, Chronic kidney disease, Vascular compliance, Albuminuria, Original Article, Articles
Abstract

Aims/Introduction: Although increases in urinary protein excretion generally precede a decline in the glomerular filtration rate, non‐proteinuric renal impairment is common in patients with diabetes. In the present study, we examined the relationship between indices of arterial stiffness and renal function in type 2 diabetic patients without proteinuria. Methods: Blood sampling, 24‐h urine collection, brachial–ankle pulse wave velocity, and 24‐h ambulatory blood pressure monitoring were performed in type 2 diabetic patients without overt proteinuria. The ambulatory arterial stiffness index was calculated as (1 – the regression slope of diastolic/systolic ambulatory blood pressure). Estimated glomerular filtration rate (eGFR)was calculated using the simplified prediction equation proposed by the Japanese Society of Nephrology. Results: Of 213 non‐proteinuric patients with type 2 diabetes, 60 (28.2%) had a reduced eGFR (

Published
2011

46. Effects of cinacalcet on achieving the targets listed in the guidelines of the Japanese Society for Dialysis Therapy

Author

Ohashi Seiji, Hatta Tsuguru, Isono Motohide, Shikano Tsutomu, Nagasaku Daisuke, Nishimura Masataka, Arimura Tetsuro, Tomita Kobin, Uzu Takashi, Nishio Toshiki, Kume Shinji, Kondo Morihiro, Nishio Toshiji, and Isshiki Keiji

Subjects
medicine.medical_specialty, Cinacalcet, Dialysis Therapy, business.industry, Urology, Medicine, business, Intensive care medicine, medicine.drug
Abstract

目的：シナカルセトによる二次性副甲状腺機能亢進症（SHPT）治療に関し，治療目標達成に影響を与える因子を検討した．対象と方法：びわこ臨床透析カンファレンス共同研究参加施設においてシナカルセト投与を受けた血液透析患者52例を対象とした．シナカルセト開始24週間観察し，日本透析医学会（JSDT）SHPT治療ガイドラインの目標値達成に関して後ろ向きに調査した．一部の症例では副甲状腺体積を超音波にて測定した．結果：治療中断した5例，intact PTH（iPTH）値の追跡不能であった1例を除く46例（平均年齢57歳，平均透析期間12年）を解析対象とした．iPTH目標値を達成したのは24例（52％）であり，iPTH，リン，カルシウムの3項目目標値をすべて達成したのは19例（41％）であった．3項目達成群は，未達成群に比し，iPTHおよびカルシウムが有意に低値であり，iPTH基礎値が500 pg/mL以下の群では，500 pg/mLを超える群に比し，高い達成率を示した（63％ vs. 11％，p＜0.001）．また，前カルシウム値が目標範囲内の群では，目標値を超えた群に比し，3項目達成率が高い傾向を示した（52％ vs. 23％，p＝0.06）．iPTH目標値を達成した24例のうち，18例（75％）が投与開始8週後以内に達成していたが，20週以降に目標値を達成した症例も存在した（3例，12.5％）．達成までの期間は前iPTH値と相関しなかった．超音波検査を行った5例では，副甲状腺総体積は投与開始前580±349 mm3から投与24週後357±254 mm3と62％減少した（p＝0.03）．結論：Ca値が目標範囲内でかつiPTHが比較的低値の症例ではシナカルセトによるJSDTガイドライン達成率が高い．また，腫大した腺腫に対してもシナカルセトは縮小効果を有する可能性が示された．

Published
2010
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47. Successful Renal Replacement Therapy for a Patient with Severe Hemophilia after Surgical Treatment of Intracranial Hemorrhage and Hydrocephalus

Author

Kato, Noriko, Chin-Kanasaki, Masami, Tanaka, Yuki, Yasuda, Mako, Yokomaku, Yukiyo, Sakaguchi, Masayoshi, Isshiki, Keiji, Araki, Shin-ichi, Ohta, Shigeru, and Uzu, Takashi

Subjects
Article Subject
Abstract

A 21-year-old Japanese male with severe hemophilia A was developed end-stage renal failure. He was placed on combination therapy with peritoneal dialysis (PD) and hemodialysis (HD). Eight months later, he developed a hypertensive cerebral hemorrhage. After emergency surgery, he was managed with PD without HD to avoid cerebral edema. One month later, his renal replacement therapy was switched to HD (three times a week) from PD, since a ventriculoperitoneal shunt catheter was placed to treat his hydrocephalus. HD could be performed safety without anticoagulant agents on condition that factor VIII is given after every HD.

Published
2011
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48. Long-Term PKC Inhibition with Oral Administration of PKC [Beta] Inhibitor Prevents Diabetic Glomerular Pathologies

Author

KOYA, DAISUKE, HANEDA, MASAKAZU, NAKAGAWA, HIROKO, ISSHIKI, KEIJI, SATO, HARUHISA, and KIKKAWA, RYUICHI

Subjects
Diabetic nephropathies -- Care and treatment, Hypoglycemic agents -- Physiological aspects, Chronic kidney failure -- Prevention, Health
Abstract

Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD) in Western and Asian society. We have previously shown that short-term treatment of streptozotocin-induced diabetic rats with PKC [Beta] [...]

Published
2000

49. Focal Segmental Glomerular Sclerosis Ameliorated by Long-term Hemodialysis Therapy with Low-density Lipoprotein Apheresis

Author

Araki, Hisazumi, primary, Ono, Shinya, additional, Nishizawa, Yuka, additional, Deji, Naoko, additional, Nakazawa, Jun, additional, Morita, Yoshikata, additional, Kume, Shinji, additional, Chin-Kanasaki, Masami, additional, Isshiki, Keiji, additional, Araki, Shin-ichi, additional, Arimura, Tetsuro, additional, Maegawa, Hiroshi, additional, and Uzu, Takashi, additional

Published
2015
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50. Peroxisome Proliferator-Activated Receptors in Diabetic Nephropathy

Author

Kume, Shinji, Uzu, Takashi, Isshiki, Keiji, and Koya, Daisuke

Subjects
Article Subject
Abstract

Diabetic nephropathy is a leading cause of end-stage renal disease, which is increasing in incidence worldwide, despite intensive treatment approaches such as glycemic and blood pressure control in patients with diabetes mellitus. New therapeutic strategies are needed to prevent the onset of diabetic nephropathy. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear transcription factors that play important roles in lipid and glucose homeostases. These agents might prevent the progression of diabetic nephropathy, since PPAR agonists improve dyslipidemia and insulin resistance. Furthermore, data from murine models suggest that PPAR agonists also have independent renoprotective effects by suppressing inflammation, oxidative stress, lipotoxicity, and activation of the renin-angiotensin system. This review summarizes data from clinical and experimental studies regarding the relationship between PPARs and diabetic nephropathy. The therapeutic potential of PPAR agonists in the treatment of diabetic nephropathy is also discussed.

Published
2008
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