Trombitás K, Jin J P, Granzier H
Central EM Laboratory, University Medical School of Pécs, Hungary.
Circ Res. 1995 Oct;77(4):856-61. doi: 10.1161/01.res.77.4.856.
One of the main contributors to passive tension of the myocardium is titin. However, it is not exactly known what portions of this approximately 1 micron-long molecule are anchored in the sarcomere (hence, are rendered inelastic) and what portions are elastic (hence, are mechanically active in developing passive tension). We assessed the length of the elastic domain of cardiac titin by ultrastructural and mechanical methods. Single cardiac myocytes were stretched by various amounts, and while in the stretched state, they were processed for immunoelectron microscopy. Several monoclonal anti-titin antibodies were used, and the locations of the titin epitopes in the sarcomere were studied as a function of sarcomere length. Only a small fraction (5% to 10%) of the approximately 1000-nm-long molecule behaved elastically under physiological conditions. This mechanically active domain is located close to the A/I junction, and its contour length when unstretched is estimated at approximately 50 to 100 nm. In sarcomeres that are slack (length approximately 1.85 microns), the mechanically active domain is folded on top of itself, and the length of the domain reaches an elastic limit of approximately 550 nm in sarcomeres that are approximately 2.9 microns long.
心肌被动张力的主要贡献者之一是肌联蛋白。然而,目前尚不清楚这个长度约为1微米的分子的哪些部分锚定在肌节中(因此变得无弹性),哪些部分是有弹性的(因此在产生被动张力时具有机械活性)。我们通过超微结构和力学方法评估了心肌肌联蛋白弹性结构域的长度。将单个心肌细胞拉伸不同程度,在拉伸状态下对其进行免疫电子显微镜处理。使用了几种抗肌联蛋白单克隆抗体,并研究了肌节中肌联蛋白表位的位置与肌节长度的关系。在生理条件下,这个长度约为1000纳米的分子中只有一小部分(5%至10%)表现出弹性。这个机械活性结构域位于靠近A/I连接处,未拉伸时其轮廓长度估计约为50至100纳米。在松弛的肌节(长度约为1.85微米)中,机械活性结构域自身折叠,在长度约为2.9微米的肌节中,该结构域的长度达到约550纳米的弹性极限。