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肌动球蛋白收缩性控制少突胶质细胞的细胞表面积。

Actomyosin contractility controls cell surface area of oligodendrocytes.

作者信息

Kippert Angelika, Fitzner Dirk, Helenius Jonne, Simons Mikael

机构信息

Max-Planck-Institute for Experimental Medicine, Hermann-Rein-Str. 3, Göttingen, Germany.

出版信息

BMC Cell Biol. 2009 Sep 25;10:71. doi: 10.1186/1471-2121-10-71.

Abstract

BACKGROUND

To form myelin oligodendrocytes expand and wrap their plasma membrane multiple times around an axon. How is this expansion controlled?

RESULTS

Here we show that cell surface area depends on actomyosin contractility and is regulated by physical properties of the supporting matrix. Moreover, we find that chondroitin sulfate proteoglycans (CSPG), molecules associated with non-permissive growth properties within the central nervous system (CNS), block cell surface spreading. Most importantly, the inhibitory effects of CSPG on plasma membrane extension were completely prevented by treatment with inhibitors of actomyosin contractility and by RNAi mediated knockdown of myosin II. In addition, we found that reductions of plasma membrane area were accompanied by changes in the rate of fluid-phase endocytosis.

CONCLUSION

In summary, our results establish a novel connection between endocytosis, cell surface extension and actomyosin contractility. These findings open up new possibilities of how to promote the morphological differentiation of oligodendrocytes in a non-permissive growth environment. See related minireview by Bauer and ffrench-Constant: http://www.jbiol.com/content/8/8/78.

摘要

背景

为了形成髓磷脂,少突胶质细胞会扩张并将其质膜多次包裹在轴突周围。这种扩张是如何控制的呢?

结果

我们在此表明,细胞表面积取决于肌动球蛋白收缩力,并受支持基质物理特性的调节。此外,我们发现硫酸软骨素蛋白聚糖(CSPG),即与中枢神经系统(CNS)内不允许生长特性相关的分子,会阻止细胞表面铺展。最重要的是,用肌动球蛋白收缩力抑制剂处理以及通过RNA干扰介导的肌球蛋白II敲低,完全消除了CSPG对质膜延伸的抑制作用。此外,我们发现质膜面积的减少伴随着液相内吞作用速率的变化。

结论

总之,我们的结果在胞吞作用、细胞表面延伸和肌动球蛋白收缩力之间建立了一种新的联系。这些发现为如何在不允许生长的环境中促进少突胶质细胞的形态分化开辟了新的可能性。见Bauer和ffrench-Constant的相关简短综述:http://www.jbiol.com/content/8/8/78

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39ef/2760528/97bdb4a6723e/1471-2121-10-71-1.jpg

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