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平衡的机械力和微管对成纤维细胞收缩的作用

Balanced mechanical forces and microtubule contribution to fibroblast contraction.

作者信息

Brown R A, Talas G, Porter R A, McGrouther D A, Eastwood M

机构信息

Tissue Repair Unit, University College London Medical School, United Kingdom.

出版信息

J Cell Physiol. 1996 Dec;169(3):439-47. doi: 10.1002/(SICI)1097-4652(199612)169:3<439::AID-JCP4>3.0.CO;2-P.

Abstract

Fibroblast locomotion is thought to generate tractional forces which lead to contraction and reorganisation of collagen in tissue development and repair. A culture force monitor device (CFM) was used to measure changes in force in fibroblast populated collagen lattices, which resulted from cytoskeletal reorganisation by cytochalasin B, colchicine, vinblastine, and taxol. Microfilament disruption abolished contraction forces, microtubule disruption elicited a new peak of contraction, while taxol stabilisation of microtubules produced a gradual fall in measured force across the collagen gel. Based on these measurements, it is suggested that the cell can be viewed as an engineering structure in which residual intracellular forces, from contractile microfilaments, exert compressive loading on microtubular elements. This microtubular structure appears to act as a "balanced space frame" (analogous to an aeroplane chassis), maintaining cell shape and consequently storing a residual internal tension (RIT). In dermal fibroblasts this hidden RIT was up to 33% of the measurable force exerted on the collagen gel. Phenotypic differences between space frame organisation and RIT levels could explain site and pathological variations in fibroblast contraction.

摘要

成纤维细胞的移动被认为会产生牵引力,这种牵引力会导致组织发育和修复过程中胶原蛋白的收缩和重组。使用一种培养力监测装置(CFM)来测量成纤维细胞填充的胶原晶格中的力变化,这些变化是由细胞松弛素B、秋水仙碱、长春花碱和紫杉醇引起的细胞骨架重组导致的。微丝破坏消除了收缩力,微管破坏引发了一个新的收缩峰值,而紫杉醇使微管稳定则导致整个胶原凝胶上测量到的力逐渐下降。基于这些测量结果,有人提出细胞可以被视为一种工程结构,其中来自收缩性微丝的残余细胞内力对微管元件施加压缩载荷。这种微管结构似乎起到了“平衡空间框架”(类似于飞机底盘)的作用,维持细胞形状并因此储存残余内部张力(RIT)。在真皮成纤维细胞中,这种隐藏的RIT高达施加在胶原凝胶上可测量力的33%。空间框架组织和RIT水平之间的表型差异可以解释成纤维细胞收缩的部位和病理变化。

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