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人骨髓间充质干细胞中与增殖相关的 K 含量变化。

Proliferation-related changes in K content in human mesenchymal stem cells.

机构信息

Department of Intracellular Signaling and Transport, Institute of Cytology, Academy of Sciences, St-Petersburg, 194064, Russian Federation.

出版信息

Sci Rep. 2019 Jan 23;9(1):346. doi: 10.1038/s41598-018-36922-y.

Abstract

Intracellular monovalent ions have been shown to be important for cell proliferation, however, mechanisms through which ions regulate cell proliferation is not well understood. Ion transporters may be implicated in the intracellular signaling: Na and Cl participate in regulation of intracellular pH, transmembrane potential, Ca homeostasis. Recently, it is has been suggested that K may be involved in "the pluripotency signaling network". Our study has been focused on the relations between K transport and stem cell proliferation. We compared monovalent cation transport in human mesenchymal stem cells (hMSCs) at different passages and at low and high densities of culture as well as during stress-induced cell cycle arrest and revealed a decline in K content per cell protein which was associated with accumulation of G1 cells in population and accompanied cell proliferation slowing. It is suggested that cell K may be important for successful cell proliferation as the main intracellular ion that participates in regulation of cell volume during cell cycle progression. It is proposed that cell K content as related to cell protein is a physiological marker of stem cell proliferation and may be used as an informative test for assessing the functional status of stem cells in vitro.

摘要

细胞内的单价离子对于细胞增殖是很重要的,然而,离子调控细胞增殖的机制尚不清楚。离子转运体可能与细胞内信号转导有关:Na+和 Cl-参与调节细胞内 pH 值、跨膜电位和 Ca2+稳态。最近,有研究表明 K+可能参与“多能性信号网络”。我们的研究集中在 K+转运与干细胞增殖之间的关系上。我们比较了不同代次、不同培养密度以及在应激诱导的细胞周期阻滞时人骨髓间充质干细胞(hMSCs)中的单阳离子转运,结果发现细胞内每蛋白的 K+含量下降,与细胞群体中 G1 期细胞的积累有关,并伴有细胞增殖速度的减慢。这表明细胞内 K+可能是成功增殖所必需的,因为它是细胞周期进展过程中参与调节细胞体积的主要细胞内离子。因此,细胞内 K+含量与细胞蛋白的比值可以作为干细胞增殖的生理标志物,并可作为评估体外干细胞功能状态的有用测试。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45d7/6344592/4b5eec1b9373/41598_2018_36922_Fig1_HTML.jpg

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