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首页> 外文期刊>Journal of Cellular Physiology >Bone morphogenetic protein-2 antagonizes bone morphogenetic protein-4 induced cardiomyocyte hypertrophy and apoptosis
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Bone morphogenetic protein-2 antagonizes bone morphogenetic protein-4 induced cardiomyocyte hypertrophy and apoptosis

机译:骨形成protein-2对抗骨头形态形成含有诱导心肌细胞肥大和凋亡

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摘要

Our previous work showed that the expression of bone morphogenetic protein-4 (BMP4) was up-regulated in pathological cardiac hypertrophy models and BMP4 induced cardiomyocyte hypertrophy and apoptosis. Bone morphogenetic protein-2 (BMP2) and BMP4 share greater than 80% amino acid homology and there exists an interaction between BMP2 and BMP4, so the aim of the present study was to elucidate the changes of BMP2 in the cardiac hypertrophy models and the effects of BMP2 on BMP4-induced cardiomyocyte hypertrophy and apoptosis. The in vivo cardiac hypertrophy models were induced by pressure-overload and swimming exercise in mice. BMP2 mRNA and protein expressions increased in pressure-overload and swimming-exercise induced cardiac hypertrophy. BMP2 itself did not elicit cardiomyocyte hypertrophy and apoptosis, but antagonized BMP4-induced cardiomyocyte hypertrophy and apoptosis. BMP2 stimulated Akt in cardiomyocytes and Akt inhibitor prevented the antagonism of BMP2 on BMP4-induced cardiomyocyte apoptosis. Furthermore, BMP2 inhibited BMP4-induced JNK activation in cardiomyocytes. In conclusion, BMP2 antagonizes BMP4-induced cardiomyocyte hypertrophy and apoptosis. The anti-apoptotic effects of BMP2 on BMP4-induced cardiomyocyte apoptosis might be through activating Akt and inhibiting JNK activation.
机译:我们以前的工作表明的表达骨形成含有(BMP4)上调病理性心脏肥大模型和BMP4诱导心肌细胞肥大和细胞凋亡。(BMP2)和BMP4份额大于80%的氨基酸同源性和存在之间的相互作用BMP2 BMP4,因此本研究的目的是阐明BMP2的变化心脏肥大模型和所带来的影响BMP2 BMP4-induced心肌细胞肥大和细胞凋亡。模型被pressure-overload和诱导游泳运动对小鼠。表达式在pressure-overload和增加swimming-exercise诱导心脏肥大。BMP2本身并不引起心肌细胞肥大和凋亡,但得罪了BMP4-induced心肌细胞肥大和细胞凋亡。和Akt抑制剂防止拮抗作用BMP2 BMP4-induced心肌细胞凋亡。此外,BMP2抑制BMP4-induced物在心肌细胞活化。对抗BMP4-induced心肌细胞肥大和凋亡。BMP2对BMP4-induced心肌细胞的影响细胞凋亡可能是通过激活一种蛋白激酶抑制物激活。

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