Sarcoplasmic reticulum genes are upregulated in mild cardiac hypertrophy but downregulated in severe cardiac hypertrophy induced by pressure overload
Sarcoplasmic reticulum genes are upregulated in mild cardiac hypertrophy but downregulated in severe cardiac hypertrophy induced by pressure overload
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DOI：
10.1006/jmcc.1996.0149
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发表时间：
1996-08-01
影响因子：
5
通讯作者：
Nagai, R
中科院分区：
文献类型：
--
作者：
Arai, M;Suzuki, T;Nagai, R
压力超负荷引起的心肌肥厚中心肌收缩和舒张特性的改变归因于细胞内Ca 2+转运的改变以及收缩蛋白的表型和数量变化。然而，矛盾的数据已被报道有关钙的摄取，释放和存储的肌浆网（SR）。本研究的目的是评价压力超负荷引起的不同程度肥厚心脏SR Ca ~（2+）-ATP酶、ryanodine受体、calsequestrin和α-actin基因表达的变化以及Ca ~（2+）摄取能力的变化。通过在肾上腹主动脉周围放置收缩夹（0.80 mm）8天，在大鼠中产生心脏肥大。mRNA水平和Ca 2+摄取能力，然后测量作为心脏肥大的严重程度的函数。轻度肥厚心肌Ca ~（2+）-ATPase和Ryanodine受体mRNA水平升高，而重度肥厚心肌Ca ~（2+）-ATPase和Ryanodine受体mRNA水平降低，呈双峰反应。Ca ~（2+）摄取能力沿着变化，与Ca ~（2+）-ATPase mRNA水平呈正相关（r=0.67，P
Changes in contractile and relaxation properties of heart muscle in the cardiac hypertrophy induced by pressure overload have been attributed to alterations in intracellular Ca2+ transport as well as the phenotypic and quantitative changes in contractile protein. However, contradictory data have been reported regarding Ca2+ uptake, release and storage by the sarcoplasmic reticulum (SR). The purpose of this study was to evaluate the changes in SR Ca2+-ATPase, ryanodine receptor, calsequestrin and alpha-actin gene expression, and the changes in Ca2+ uptake capacity in various degrees of hypertrophied hearts due to pressure overload. Cardiac hypertrophy was produced in rats by placing a constricting clip (0.80 mm) around the suprarenal abdominal aorta for 8 days. The mRNA levels and Ca2+ uptake capacity were then measured as a function of the severity of cardiac hypertrophy. Ca2+-ATPase and ryanodine receptor mRNA levels were increased in mildly hypertrophied hearts but were diminished in severely hypertrophied hearts, showing a bimodal response to pressure overload, Ca2+ uptake capacity showed similar changes along with a positive correlation with Ca2+-ATPase mRNA level (r=0.67, P