Detection of mRNAscharacteristically expressed in heart failure transiti
Detection of mRNAscharacteristically expressed in heart failure transiti
批准号:
10670646
负责人:
KIHARA Yasuki
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
项目状态:
已结题
起止时间:
1998 至 1999
中文摘要
利用达尔盐敏感大鼠,我们最近建立了一种动物模型,以可重复的方式观察到从机械代偿的同心型左室肥大到其失代偿伴左室功能障碍和扩大的转变。在本研究中,我们通过差异显示RT-PCR (DD)方法,探讨了代偿性LVH和LV衰竭阶段心肌mRNA表达的明显差异。通过DD比较,我们检测到130个mRNA片段,并成功进行了TA克隆。随后的同源性搜索显示,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等mrna。有趣的是,有几种mrna的编码因子被认为与心力衰竭或心脏重构无关。因此,我们将阐明这些mrna编码的因子在心力衰竭中的病理生理作用。
英文摘要
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.
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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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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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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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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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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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共 24 条
Metabolic Cardiomyopathy: Disease Entity and Pathophysiology
-
批准号:24591055
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.24万
-
财政年份:2012
-
负责人:KIHARA Yasuki
-
依托单位:
Isozyme-Specific Pharmacological Properties of Protein Kinase C and Approaches to New Drug Development
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批准号:15390245
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$6.02万
-
财政年份:2003
-
负责人:KIHARA Yasuki
-
依托单位:
Identification of myocardial Tissue Tactors of ventricular remodeling
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批准号:13670706
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.3万
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财政年份:2001
-
负责人:KIHARA Yasuki
-
依托单位:
Cross Talk Between Protein Kinase C and Intracellular Calcium in the Cardiomyocyte
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批准号:06454291
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$3.14万
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财政年份:1994
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负责人:KIHARA Yasuki
-
依托单位:
海外基金