Detection of mRNAscharacteristically expressed in heart failure transiti

心力衰竭转折过程中特征性表达的mRNA检测

基本信息

  • 批准号:
    10670646
  • 负责人:
  • 金额:
    $ 2.37万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1998
  • 资助国家:
    日本
  • 起止时间:
    1998 至 1999
  • 项目状态:
    已结题

项目摘要

Using Dahl salt-sensitive rats, we recently developed an animal model in which transition from mechanically compensated concentric LV hypertrophy to its decompensation with LV dysfunction and enlargement was observed in a reproducible manner. In the present study, we explored myocardial mRNA expressions that showed distinct difference between the stages of compensated LVH and LV failure, by means of differential display RT-PCR (DD) methods. We detected 130 mRNA fragments along with the DD comparison and these mRNAs were successfully TA cloned. The subsequent homology search reveled that they consisted of 23 know genes and 14 unknown genes. In the known gene group, mRNAs coding such as atrial natriuretic peptide and alpha-cardiac MHC were found. Interestingly, there were several mRNAs that code factors having been assumed to be independent of heart failure or cardiac remodeling. Thus, we are going to elucidate the pathophysiological roles of these factors coded by these mRNAs on the heart failure.
使用Dahl盐敏感大鼠,我们最近开发了一种动物模型,在该模型中,以可重复的方式观察到从机械代偿向心性LV肥大到其失代偿伴LV功能障碍和增大的过渡。在本研究中,我们探讨心肌mRNA表达的代偿性LVH和LV衰竭的阶段之间的显着差异,通过差异显示RT-PCR(DD)方法。我们检测到130个mRNA片段沿着与DD比较,这些mRNA成功地TA克隆。同源性分析表明,它们由23个已知基因和14个未知基因组成。在已知的基因组中,发现了编码心房利钠肽和α-心脏MHC的mRNA,有趣的是,有几个编码因子的mRNA被认为与心力衰竭或心脏重塑无关。因此,我们将阐明由这些mRNA编码的这些因子在心力衰竭中的病理生理作用。

项目成果

期刊论文数量(24)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Fujita M, Kihara Y, Hasegawa K, et al.: "Heparin potentiates collateral growth but not growth of intramyocardial endarteries in dogs with repeated coranary occlusion"International J Cardiol. 70. 165-170 (1999)
Fujita M、Kihara Y、Hasekawa K 等人:“肝素可增强冠状动脉反复闭塞犬的侧支生长,但不会增强心肌内动脉的生长”International J Cardiol。
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    0
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Fujita M,Nakae I,Kihara Y et al.: "Determinants of collateral development in patients with acute myocardial infarction"Clin Cardiol. 22. 595-599 (1999)
Fujita M、Nakae I、Kihara Y 等:“急性心肌梗死患者侧枝发育的决定因素”Clin Cardiol。
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    0
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Sakayama S, Matsumori A, Kihara Y, et al.: "New insights into the path ophysiological role for cytokinesin heart failure"Cardiovasc Res. 42. 557-564 (1999)
Sakayama S、Matsumori A、Kihara Y 等人:“对细胞因子心力衰竭路径生理学作用的新见解”Cardiovasc Res。
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    0
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Ikemoto M, Hasegawa K, Kihara Y, et al.: "Development of enzyme-linked immuno-sorbent assay for acidic fibroblast growth and its clinical application."Clin Chim Acta. 283. 171-182 (2000)
Ikemoto M、Hasekawa K、Kihara Y 等人:“酸性成纤维细胞生长酶联免疫吸附测定法的开发及其临床应用。”Clin Chim Acta。
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    0
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木原康樹,篠山重咸: "合併症を伴った高血圧症の治療,心疾患:心肥大"日本臨床:2000年増刊「高血圧症」. 312-315 (2000)
Yasuki Kihara、Shigeaki Shinoyama:“治疗高血压并发症、心脏病:心脏肥大”日本临床:2000 年特刊“高血压”312-315 (2000)。
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    0
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KIHARA Yasuki其他文献

KIHARA Yasuki的其他文献

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{{ truncateString('KIHARA Yasuki', 18)}}的其他基金

Metabolic Cardiomyopathy: Disease Entity and Pathophysiology
代谢性心肌病:疾病实体和病理生理学
  • 批准号:
    24591055
  • 财政年份:
    2012
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Isozyme-Specific Pharmacological Properties of Protein Kinase C and Approaches to New Drug Development
蛋白激酶 C 同工酶特异性药理学特性和新药开发方法
  • 批准号:
    15390245
  • 财政年份:
    2003
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Identification of myocardial Tissue Tactors of ventricular remodeling
心室重构心肌组织因子的鉴定
  • 批准号:
    13670706
  • 财政年份:
    2001
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Cross Talk Between Protein Kinase C and Intracellular Calcium in the Cardiomyocyte
心肌细胞中蛋白激酶 C 和细胞内钙之间的串扰
  • 批准号:
    06454291
  • 财政年份:
    1994
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)

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