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单个心肌肌原纤维中肌联蛋白伸展的限度。

Limits of titin extension in single cardiac myofibrils.

作者信息

Linke W A, Bartoo M L, Ivemeyer M, Pollack G H

机构信息

Institute of Physiology II, University of Heidelberg, Germany.

出版信息

J Muscle Res Cell Motil. 1996 Aug;17(4):425-38. doi: 10.1007/BF00123359.

Abstract

Passive force and dynamic stiffness were measured in relaxed, single myofibrils from rabbit ventricle over a wide range of sarcomere lengths, from approximately 2-5 microns. Myofibril stretch up to sarcomere lengths of approximately 3 microns resulted in a steady increase in both force and stiffness. The shape of the length-force and the length-stiffness curves remained fully reproducible for repeated extensions to a sarcomere length of approximately 2.7 microns. Above this length, myofibrillar viscoelastic properties were apparently changed irreversibly, likely due to structural alterations within the titin (connectin) filaments. Stretch beyond approximately 3 microns sarcomere length resulted in a markedly reduced slope of the passive force curve, while the stiffness curve became flat. Thus, cardiac sarcomeres apparently reach a strain limit near a length of 3 microns. Above the strain limit, both curve types frequently showed a series of inflections, which we assumed to result from the disruption of titin-thick filament bonds and consequent addition of previously bound A-band titin segments to the elastic I-band titin portion. Indeed, we confirmed in immunofluorescence microscopic studies, using a monoclonal antibody against titin near the A/I junction, that upon sarcomere stretch beyond the strain limit length, the previously stationary antibody epitopes suddenly moved into the I-band, indicating A-band titin release. Altogether, the passive force/stiffness-length relation of cardiac myofibrils was qualitatively similar to, but quantitatively different from, that reported for skeletal myofibrils. From these results, we inferred that cardiac myofibrils have an approximately two times greater relative I-band titin extensibility than skeletal myofibrils. This could hint at differences in the maximum passive force-bearing capacity of titin filaments in the two muscle types.

摘要

在兔心室的松弛单根肌原纤维中,于大约2 - 5微米的广泛肌节长度范围内测量了被动力和动态刚度。肌原纤维拉伸至大约3微米的肌节长度时,力和刚度均持续增加。对于重复拉伸至大约2.7微米的肌节长度,长度 - 力曲线和长度 - 刚度曲线的形状完全可重复。超过此长度,肌原纤维的粘弹性特性显然发生了不可逆变化,可能是由于肌联蛋白(连接蛋白)丝内的结构改变所致。肌节长度超过大约3微米的拉伸导致被动力曲线的斜率显著降低,而刚度曲线变得平坦。因此,心脏肌节显然在接近3微米的长度处达到应变极限。超过应变极限后,两种曲线类型经常出现一系列拐点,我们认为这是由于肌联蛋白 - 粗肌丝键的破坏以及随后将先前结合的A带肌联蛋白片段添加到弹性I带肌联蛋白部分所致。实际上,我们在免疫荧光显微镜研究中使用针对A/I交界处附近肌联蛋白的单克隆抗体证实,当肌节拉伸超过应变极限长度时,先前静止的抗体表位突然移入I带,表明A带肌联蛋白释放。总体而言,心脏肌原纤维的被动力/刚度 - 长度关系在质量上与骨骼肌原纤维报道的相似,但在数量上不同。从这些结果我们推断,心脏肌原纤维的相对I带肌联蛋白伸展性比骨骼肌原纤维大约大两倍。这可能暗示了两种肌肉类型中肌联蛋白丝的最大被动承载能力存在差异。

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