Molecular biological changes of ADP/ATP carrier in cardiomypathic hamster

心肌病仓鼠ADP/ATP载体的分子生物学变化

• 批准号: 06670745
• 负责人: KATO Mitsutoshi
• 金额: $ 1.09万
• 依托单位: Jikei University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670745/
• 关键词: ADP; ATP carrier; J-2-N strain; Cardiomyopathic hamster; ATP Carrier protein; cardiomyopathic hamster

ADP/ATP carrier protein (AAC) is an integral protein present in the inner mitochondrial membrane that performs the exchange of cytoplasmic and intramitochondrial ADP and ATP.AAC content of myocardium was studied in J-2-N cardiomyopathic hamsters. The AAC content was significantly decreased in the J-2-N hamsters. By molecular biological analysis, hamster AAC cDNA was cloned by the plaque hybridization method. The AAC cDNA hybridized specifically with AAC mRNA,so RNA dot-blot hybridization was performed. The highest AAC mRNA level was observed in control hamsters followed by J-2-N hamsters with mild myocardial damage, J-2-N hamsters with severe myocardial damage and Bio 14.6 cardiomyopathic hamsters. These results suggest that a decreased AAC content may contribute to the pathogenesis of cardiomyopathy and that a decrease of AAC mRNA levels may explain the abnormalities of AAC in J-2-N cardiomyopathic hamsters.

ADP/ATP 载体蛋白 (AAC) 是存在于线粒体内膜中的整合蛋白，负责细胞质和线粒体内 ADP 和 ATP 的交换。在 J-2-N 心肌病仓鼠中研究了心肌的 AAC 含量。 J-2-N仓鼠的AAC含量显着降低。通过分子生物学分析，采用噬菌斑杂交法克隆了仓鼠AAC cDNA。 AAC cDNA与AAC mRNA特异性杂交，进行RNA斑点杂交。在对照仓鼠中观察到最高的 AAC mRNA 水平，其次是具有轻度心肌损伤的 J-2-N 仓鼠、具有严重心肌损伤的 J-2-N 仓鼠和 Bio 14.6 心肌病仓鼠。这些结果表明，AAC 含量的降低可能导致心肌病的发病机制，并且 AAC mRNA 水平的降低可以解释 J-2-N 心肌病仓鼠中 AAC 的异常。

项目成果

Nagano M,Kato M.: "Pathophysiological Aspects of the Cardioimyopathic J-2-N Hamster." The Cardiomyopathic Heart.157-164 (1994)

Nagano M，Kato M.：“心肌病 J-2-N 仓鼠的病理生理学方面。”

KATO M: "Molecular biological changes of adenine nucleotide translocator in J-2-N cardiomyopathic hamsters" Mechanisms of Heart Failure. (in press). (1995)

加藤 M：“J-2-N 心肌病仓鼠中腺嘌呤核苷酸易位子的分子生物学变化”心力衰竭的机制。

Takeda N,Kato M.: "Pharmacological modulation of cardiac hypertrophy in hypertensive patients." Raven Press,New York. The Adapted Heart.403-414 (1994)

Takeda N，Kato M.：“高血压患者心脏肥大的药理学调节。”

KATO M: "Quantitative abnormalities of ADP/ATP carrier protein in cardiomyopathic hamsters." The Adaptes Heart. Chap7. 91-98 (1994)

KATO M：“心肌病仓鼠中 ADP/ATP 载体蛋白的数量异常。”

KATO M: "Molecular biological changes of adenine nucleotide translocator in J-2-N cardiomyopathic hamsters" Mechanisms of Heart Failure. 197-202 (1994)

加藤 M：“J-2-N 心肌病仓鼠中腺嘌呤核苷酸易位子的分子生物学变化”心力衰竭的机制。