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源自MDCK II细胞的跨孔顶端细胞膜的弹性特性

Elastic Properties of Pore-Spanning Apical Cell Membranes Derived from MDCK II Cells.

作者信息

Nehls Stefan, Janshoff Andreas

机构信息

Georg-August-Universität Göttingen, Institute of Physical Chemistry, Göttingen, Germany.

Georg-August-Universität Göttingen, Institute of Physical Chemistry, Göttingen, Germany.

出版信息

Biophys J. 2017 Oct 17;113(8):1822-1830. doi: 10.1016/j.bpj.2017.08.038.

Abstract

The mechanical response of adherent, polarized cells to indentation is frequently attributed to the presence of an endogenous actin cortex attached to the inner leaflet of the plasma membrane. Here, we scrutinized the elastic properties of apical membranes separated from living cells and attached to a porous mesh in the absence of intracellular factors originating from the cytosol, organelles, the substrate, neighbors, and the nucleus. We found that a tension-based model describes the data very well providing essentially the prestress of the shell generated by adhesion of the apical membrane patches to the pore rim and the apparent area compressibility modulus, an intrinsic elastic modulus modulated by the surface excess stored in membrane reservoirs. Removal of membrane-associated proteins by proteases decreases the area compressibility modulus, whereas fixation and cross-linking of proteins with glutaraldehyde increases it.

摘要

贴壁极化细胞对压痕的机械响应通常归因于存在附着于质膜内小叶的内源性肌动蛋白皮层。在此,我们仔细研究了从活细胞分离并附着于多孔网的顶端膜的弹性特性,此时不存在源自细胞质、细胞器、底物、相邻细胞和细胞核的细胞内因子。我们发现基于张力的模型能很好地描述这些数据,该模型本质上提供了顶端膜片与孔边缘粘附所产生的壳的预应力以及表观面积压缩模量,这是一种由膜储存器中储存的表面过剩物质调节的固有弹性模量。用蛋白酶去除膜相关蛋白会降低面积压缩模量,而用戊二醛固定和交联蛋白则会增加该模量。

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