Roles of interstitial cells on the recovery process from acute renal failure
| Project/Area Number |
13671107
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Hamamatsu University, School of Medicine |
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Principal Investigator |
FUJIGAKI Yoshihide Hamamatsu Univ. Sch. Of Med. 1st Dept. of Med., Research Associate, 医学部, 助手 (20283351)
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| Co-Investigator(Kenkyū-buntansha) |
HISHIDA Akira Hamamatsu Univ. Sch. Of Med. 1st Dept. of Med., Professor, 医学部, 教授 (70111812)
YONEMURA Katsuhiko Hamamatsu Univ. Sch. Of Med. Hemodialysis Unit, Associate Professor, 医学部附属病院, 助教授 (40252176)
KATO Akihiko Hamamatsu Univ. Sch. Of Med. 1st Dept. of Med., Research Associate, 医学部附属病院, 助手 (60324357)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | acute renal failure / myofibroblast / alpha-smooth muscle actin / macrophage / cellular fibronectin / mycophenolate mofetil / uranyl acetate / 細胞性フィブロネクチン / ミコフェノール酸モフュチル / 尿細管細胞 / 尿細管増殖 / ミィオフィブロブラスト / mycophenolate mofetil |
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| Research Abstract |
1. We reported that in uranyl acetate (UA)-induced acute renal failure (ARF) in rats, transient infiltration of macrophages and α-smooth muscle actin-positive myofibroblasts in the interstitium occurred in associalion with the peak activity of tubular regeneration after acute tubular injury and that the regeneration of tubular epithelial cells was inhibited by the suppression of the interstitial cellular response by mycophenolate mofetil. Based on the findings we concluded that myofibroblasts and infiltrating macrophages may contribute as in the wound healing process to cellular recovery in this ARF model.
2. Mechanical tension judged by tubular dilatation may contribute to induce α-smooth muscle actin phenotype in association with stress fiber formation and intercellular junctions in fibroblastic cells to adjust tensional homeostasis and not to collapse the damaged nephron structures. Myofibroblasts may furnish cellular fibronectin to condition an environment for tubular proliferation.
… More
Fibronectin may be the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins). Moreover, myofibroblasts can provide growth factors in autocrine and/or paracrine fashion.
3. Macrophages can produce several types of cytokines and growth factors, which promote epithelial cell proliferation. Macrophages may also function as scavengers and phagocytose cellular debris in the tubular lumen, cleaning the wound site to promote healing. Macrophaes that accumulated in the vicinity of the tubular basement membrane might act as outpost of the defense system to monitor incoming antigens.
4. Although renal interstitial myofibroblasts and macrophages have often been regarded rather harmful in clinical and experimental settings as they are considered as indicators of interstitial fibrosis, the roles of myofibroblasts and macrophages in this ARF seemed to be all necessary components of wound healing. Further analysis of transient response of these interstitial cellular factors would be useful to explore the mechanisms of kidney repair and fibrosis. Less
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Report
(3 results)
Research Products
(6 results)
