GLOMERULAR CAPILLARY WALL--NORMAL AND PATHOLOGIC
肾小球毛细血管壁——正常和病理
基本信息
- 批准号:2905255
- 负责人:
- 金额:$ 30万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1991
- 资助国家:美国
- 起止时间:1991-04-01 至 2003-08-31
- 项目状态:已结题
- 来源:
- 关键词:diabetic nephropathy epithelium gene environment interaction gene expression genetically modified animals glucose metabolism histogenesis immunocytochemistry immunoprecipitation in situ hybridization laboratory mouse mammalian embryology mesenchyme pathologic process polymerase chain reaction representational difference analysis transfection
项目摘要
DESCRIPTION (Adapted from Investigator's Abstract): The overall objective
of this proposal is to study the pathogenetic mechanisms involved in
diabetic induced lesions in the embryonic metanephros. Three potential
target genes will be examined mesodermal specific cDNA(MEST), H19, and
TIN-Ag based on the spatio-temporal expression of these genes with MEST
expressed in the metanephric mesenchyme H19 in the ureteric bud epithelia
and TIN-Ag in an anti-polar proximal expression opposite that of H19 in the
S-shaped body suggesting the three molecules are interlinked in early
nephric development. Experiments are proposed under five specific aims to
study the normal and abnormal biology of these molecules during renal
development. I. Spatio-temporal expression of MEST, H19 and TIN-Ag during
metanephric development will be investigated by using in situ hybridization,
competitive PCR, immunohistochemical and immunoprecipitation methods. II.
Their role in epithelial: mesenchymal interactions, prevalent during
metanephrogenesis, will be assessed by antibody, antisense, transgene and
transfection experiments. III. Molecular protein: protein and RNA:
protein interactions will be investigated by using recombinant fusion
proteins of various constructs of these three molecules. IV. Alterations
in these molecules will be investigated during elevated concentration of
glucose in vitro and in hyperglycemia. V. Finally, the
hyperglycemia-induced/suppressed genes during embryonic renal development
will be investigated using RDA and Serial Analysis of Gene Expression
(SAGE).
描述(改编自研究者摘要):总体目标
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Yashpal S. Kanwar其他文献
myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience :a new mechanism relevant to the pathogenesis of diabetic nephropathy.
肌醇加氧酶过度表达会加速活性氧的产生并加剧高血糖环境下的细胞损伤——与糖尿病肾病发病机制相关的新机制。
- DOI:
- 发表时间:
2016 - 期刊:
- 影响因子:0
- 作者:
Lin Sun;Rajesh K. Dutta;Ping Xie;Yashpal S. Kanwar - 通讯作者:
Yashpal S. Kanwar
Hyperglycemia: its imminent effects on mammalian nephrogenesis
- DOI:
10.1007/s00467-005-1888-7 - 发表时间:
2005-05-05 - 期刊:
- 影响因子:2.600
- 作者:
Yashpal S. Kanwar;Baibaswata Nayak;Sun Lin;Shigeru Akagi;Ping Xie;Jun Wada;Sumant S. Chugh;Farhad R. Danesh - 通讯作者:
Farhad R. Danesh
Yashpal S. Kanwar的其他文献
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{{ truncateString('Yashpal S. Kanwar', 18)}}的其他基金
Pathobiology of HMG-CoA reductase inhibitors in diabetes
HMG-CoA 还原酶抑制剂在糖尿病中的病理学
- 批准号:
6707485 - 财政年份:2003
- 资助金额:
$ 30万 - 项目类别:
Pathobiology of HMG-CoA reductase inhibitors in diabetes
HMG-CoA 还原酶抑制剂在糖尿病中的病理学
- 批准号:
6855801 - 财政年份:2003
- 资助金额:
$ 30万 - 项目类别:
Pathobiology of HMG-CoA reductase inhibitors in diabetes
HMG-CoA 还原酶抑制剂在糖尿病中的病理学
- 批准号:
7017008 - 财政年份:2003
- 资助金额:
$ 30万 - 项目类别:
Pathobiology of HMG-CoA reductase inhibitors in diabetes
HMG-CoA 还原酶抑制剂在糖尿病中的病理学
- 批准号:
6599152 - 财政年份:2003
- 资助金额:
$ 30万 - 项目类别:
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