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心肌营养素-1可诱导培养的心肌细胞中热休克蛋白的积累,并保护它们免受应激刺激。

Cardiotrophin-1 induces heat shock protein accumulation in cultured cardiac cells and protects them from stressful stimuli.

作者信息

Stephanou A, Brar B, Heads R, Knight R D, Marber M S, Pennica D, Latchman D S

机构信息

Department of Molecular Pathology, Windeyer Institute of Medical Sciences, University College London Medical School, UK.

出版信息

J Mol Cell Cardiol. 1998 Apr;30(4):849-55. doi: 10.1006/jmcc.1998.0651.

Abstract

Cardiotrophin-1 (CT-1) was originally identified as a molecule capable of inducing cardiac hypertrophy. We show here that treatment of cultured neonatal cardiocytes with CT-1 induces enhanced synthesis of the heat shock proteins hsp70 and hsp90, with hsp70 levels being enhanced three-fold and hsp90 levels being enhanced seven-fold. Such CT-1-treated cells are protected against subsequent exposure to severe thermal or ischaemic stress, as assayed both by measures of total cell death, such as trypan blue exclusion and LDH release, and by measures of apoptosis, such as propidium-iodide-staining and TUNEL-labelling. Hence, CT-1 can induce the protective hsps and protect cardiac cells from diverse stresses.

摘要

心肌营养素-1(CT-1)最初被鉴定为一种能够诱导心肌肥大的分子。我们在此表明,用CT-1处理培养的新生心肌细胞可诱导热休克蛋白hsp70和hsp90的合成增强,其中hsp70水平提高了三倍,hsp90水平提高了七倍。通过诸如台盼蓝排斥法和乳酸脱氢酶释放等总细胞死亡测量方法,以及诸如碘化丙啶染色和TUNEL标记等凋亡测量方法检测发现,经CT-1处理的此类细胞在随后暴露于严重热应激或缺血应激时受到保护。因此,CT-1可诱导保护性热休克蛋白的产生,并保护心肌细胞免受多种应激的影响。

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