Apoptosis of Neutrophils in Uremia
尿毒症中性粒细胞凋亡
基本信息
- 批准号:6669117
- 负责人:
- 金额:$ 5.39万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2002
- 资助国家:美国
- 起止时间:2002-09-30 至 2004-08-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION: (provided by applicant): In the U.S., infection is a leading cause
of death among patients with chronic renal failure (CRF). This is due in part
to the immune deficiency of the uremic syndrome. In the past decade, apoptosis or programmed cell death (PCD) has been the subject of intense investigation.
In contrast to necrosis, apoptosis is a programmed, active and highly selective
death mechanism, allowing for the removal of redundant or excessively damaged
cells. It is an essential component of development and cellular regulation, and
in both excessive and reduced amount, has pathophysiological and therapeutic
implications. In CRF, polymorphonuclear leukocytes (PMN) undergo accelerated
PCD. The long-term goals of this proposal are to elucidate the cellular and
molecular pathways governing PMN apoptosis in CRF. The studies will
specifically concentrate on three major signaling pathways: the Fas/FasL
system, the Bax/Bc12 system and oxidative stress. The studies will utilize PMN
(healthy subjects and patients with CRF) and HL-60 granulocytes. Apoptosis
induction models will use receptor- and stress-mediated stimuli (anti-Fas
antibodies, pro-oxidant agents, dialysis membranes, uremic toxins, etc). The
results are expected to enhance our understanding of leukocyte biology in CRF,
and lay the foundation for developing novel strategies to combat immune
dysfunction in CRF.
描述:(由申请人提供):在美国,感染是主要原因
慢性肾功能衰竭(CRF)患者的死亡率。部分原因
尿毒症综合症的免疫缺陷在过去的十年中,细胞凋亡或程序性细胞死亡(PCD)一直是激烈的研究主题。
与坏死不同,凋亡是一种程序性、主动性和高度选择性的细胞凋亡。
死亡机制,允许去除多余的或过度损坏的
细胞它是发育和细胞调节的重要组成部分,
无论过量还是减量,
含义。在CRF中,多形核白细胞(PMN)经历加速的
PCD。这项提案的长期目标是阐明细胞和
CRF中中性粒细胞凋亡的分子调控途径。这些研究将
具体集中在三个主要的信号通路:Fas/FasL
Bax/Bc 12系统和氧化应激。研究将使用PMN
(健康受试者和CRF患者)和HL-60粒细胞。凋亡
诱导模型将使用受体和应激介导的刺激(抗Fas
抗体、促氧化剂、透析膜、尿毒症毒素等)。的
预期结果将增强我们对CRF中白细胞生物学的理解,
并为开发新的对抗免疫系统的策略奠定基础。
慢性肾衰竭功能障碍。
项目成果
期刊论文数量(0)
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MARY C PERIANAYAGAM其他文献
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{{ truncateString('MARY C PERIANAYAGAM', 18)}}的其他基金
Oxidative Stress Related Gene Polymorphisms in Acute kidney Injury
急性肾损伤氧化应激相关基因多态性
- 批准号:
7808021 - 财政年份:2009
- 资助金额:
$ 5.39万 - 项目类别:
Oxidative Stress Related Gene Polymorphisms in Acute kidney Injury
急性肾损伤氧化应激相关基因多态性
- 批准号:
8056099 - 财政年份:2009
- 资助金额:
$ 5.39万 - 项目类别:
Oxidative Stress Related Gene Polymorphisms in Acute kidney Injury
急性肾损伤氧化应激相关基因多态性
- 批准号:
7641201 - 财政年份:2009
- 资助金额:
$ 5.39万 - 项目类别: