Regenerative Medicine of Nephron Segments
肾单位节段再生医学
基本信息
- 批准号:15390265
- 负责人:
- 金额:$ 9.41万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 财政年份:2003
- 资助国家:日本
- 起止时间:2003 至 2006
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Ischemic acute renal failure (ARF) is the most common form of ARF in the adult population. The molecular mechanisms of tubular regeneration after ischemic renal injury remain largely unknown. It has been suggested that regeneration processes may recapitulate developmental processes in order to restore organ or tissue function. The adult tubular epithelial cells have a potent ability of regenerate after cellular damage. We examined functional role of two developmental genes, Wnt-4 and Ets-1 in renal tubular regeneration in ARF. This slide shows hypothesis of mechanisms of renal tubular regeneration. After renal tubular injury, such as ischemia, renal tubular cells falls into apoptosis or necrosis. Then, some parts of injured renal tubules regenerate. We hypothesized three possibilities of renal tubular regeneration. One is the presence of renal tubular stem cells. Concerning to the stem cells, mamy presentation have already been reported in this meeting. The second possibility is Dedifferentiation. Our hypothesis is that the renal tubular cells transform to dedifferentiated cells, which have embryonic character, such as expression of Wnt-4 and Ets-1. The other possibility is involvement of blood cells.In summary, we demonstrated that when the renal tubular cells are damaged, several recovery mechanisms are occurs using many types of stem cells. We may improve the recovery of renal tubular damage by manipulating stem cells such as tissue specific stem cells, or dedifferentiated stem cells, bone-marrow deribed stein cells, or ES cells. Further understanding of renal regeneration will improve new therapeutic strategy for ARF.
缺血性急性肾衰竭(ARF)是成人人群中最常见的ARF形式。缺血性肾损伤后肾小管再生的分子机制仍不清楚。有人认为,再生过程可能重演发育过程,以恢复器官或组织的功能。成人肾小管上皮细胞在细胞损伤后具有较强的再生能力。我们研究了两个发育基因Wnt-4和Ets-1在ARF肾小管再生中的功能作用。这张幻灯片显示了肾小管再生机制的假设。肾小管损伤后,如缺血,肾小管细胞福尔斯发生凋亡或坏死。然后,受损肾小管的部分再生。我们假设了肾小管再生的三种可能性。一个是肾小管干细胞的存在。关于干细胞,我的报告已经在这次会议上作了汇报。第二种可能是去分化。我们的假设是,肾小管细胞转化为去分化细胞,具有胚胎特征,如Wnt-4和Ets-1的表达。总之,我们证明了当肾小管细胞受损时,使用多种类型的干细胞会发生几种恢复机制。我们可以通过操纵干细胞如组织特异性干细胞、去分化干细胞、骨髓源性干细胞或ES细胞来改善肾小管损伤的恢复。对肾再生的进一步认识将为ARF的治疗提供新的策略。
项目成果
期刊论文数量(12)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
尿細管性アシドーシスとその他のまれな尿細管疾患、今日の治療指針
肾小管性酸中毒等罕见肾小管疾病,今日治疗指南
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:寺田 典生;田中 啓之;佐々木 成;Y.Terada et al.;T.Yokoo et al.;Y.Oyama et al.;T.Kobayashi et al.;H.Tanaka et al.;T.Wada et al.;寺田典生
- 通讯作者:寺田典生
Human mesanchymal stem cells in rodent whole-embryo culture are reprogrammed to contribute to kidney tissues.
啮齿动物全胚胎培养中的人类间充质干细胞被重新编程以促进肾组织的形成。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:T.Yokoo;T.Ohashi;JS.Shen;K.Sakurai;Y.Miyazaki;Y.Utsunomiya;M.Takahashi;Y.Terada;Y.Eto;T.Kawamura;T.Hosoya
- 通讯作者:T.Hosoya
Shimamura H et al.: "The PI3-kinase-Akt pathway promotes mesangial cell survival and inhibited apoptosis in vitro via NF-kB and Bad"J Am Soc Nephrol. 14. 1427 (2003)
Shimamura H 等人:“PI3-激酶-Akt 途径通过 NF-kB 和 Bad 在体外促进系膜细胞存活并抑制细胞凋亡”J Am Soc Nephrol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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TERADA Yoshio其他文献
TERADA Yoshio的其他文献
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{{ truncateString('TERADA Yoshio', 18)}}的其他基金
Regulation of mitochondrial function for protection of acute kidney
调节线粒体功能以保护急性肾
- 批准号:
15K15331 - 财政年份:2015
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Mitophagy and acute kidney injury
线粒体自噬和急性肾损伤
- 批准号:
25670412 - 财政年份:2013
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Regulation of autophagy in acute kidney injury treatment
急性肾损伤治疗中自噬的调控
- 批准号:
23390227 - 财政年份:2011
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Involvement of autopgaly and lysosomal system in renal diseases
自噬和溶酶体系统参与肾脏疾病
- 批准号:
21659214 - 财政年份:2009
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Therapeutic approach for kidney diseases by regenerative medicine
再生医学治疗肾脏疾病的方法
- 批准号:
19390229 - 财政年份:2007
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
GENE THERAPY OD ACUTE RENAL FAILURE BY CELL CYCLE-REGULATED GENES
通过细胞周期调控基因治疗急性肾衰竭
- 批准号:
12671029 - 财政年份:2000
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Mechanisms and regulation of renal urinary concentration
肾尿浓度的机制和调节
- 批准号:
09307022 - 财政年份:1997
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
GENE THERAPY OF GLOMERULONEPHRITIS BY GENE TRANSFER OF CELL CYCLE-RELATED GENES.
通过细胞周期相关基因的基因转移进行肾小球肾炎的基因治疗。
- 批准号:
09557090 - 财政年份:1997
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for Scientific Research (B).
Molecular approaches to the pathogenesis of glomerulanephritis by vasoactive substances
血管活性物质对肾小球肾炎发病机制的分子研究
- 批准号:
05837007 - 财政年份:1993
- 资助金额:
$ 9.41万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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