Suppr超能文献

正常人成纤维细胞的衰老与离子型谷氨酸受体GluR6/Grik2的表达有关。

Senescence of Normal Human Fibroblasts Relates to the Expression of Ionotropic Glutamate Receptor GluR6/Grik2.

作者信息

Zhawar Vikramjit K, Kandpal Raj P, Athwal Raghbir S

机构信息

Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, U.S.A.

Department of Basic Medical Sciences, Western University of Health Sciences, Pomona, CA, U.S.A.

出版信息

Cancer Genomics Proteomics. 2020 Nov-Dec;17(6):707-714. doi: 10.21873/cgp.20225.

Abstract

BACKGROUND/AIM: Glutamate receptor GRIK2, previously designated as GluR6, is best described in neuronal cells. However, its biological relevance in non-neuronal cells is not well understood. We have investigated the expression of this important protein in normal human fibroblasts as a function of cell proliferation.

MATERIALS AND METHODS

We introduced expression constructs of all five isoforms (A-E) of GRIK2 in normal human fibroblasts and investigated the cells for the presence and localization of GRIK2, as well as for cell proliferation and senescence over a period of 24 days.

RESULTS

The expression of GRIK2-A isoform led to immediate cessation of cell proliferation. However, the cell numbers increased by 1.5- to 9.0-fold in 24 days upon transfection with B, C, D and E isoforms, after which they entered a state of senescence. The decreased proliferation was reflected by incorporation of BrdU in only 2-8% of transfected cells even after culturing them for 16 days.

CONCLUSION

Our results are indicative of an association between GRIK2 and aging of fibroblasts.

摘要

背景/目的:谷氨酸受体GRIK2,以前称为GluR6,在神经元细胞中研究得最为深入。然而,其在非神经元细胞中的生物学相关性尚未得到充分了解。我们研究了这种重要蛋白质在正常人成纤维细胞中的表达与细胞增殖的关系。

材料与方法

我们将GRIK2的所有五种亚型(A - E)的表达构建体导入正常人成纤维细胞,并在24天内研究细胞中GRIK2的存在、定位以及细胞增殖和衰老情况。

结果

GRIK2 - A亚型的表达导致细胞增殖立即停止。然而,用B、C、D和E亚型转染后,细胞数量在24天内增加了1.5至9.0倍,之后进入衰老状态。即使在培养16天后,只有2 - 8%的转染细胞掺入BrdU,这反映了增殖的减少。

结论

我们的结果表明GRIK2与成纤维细胞衰老之间存在关联。

相似文献

3
Genomic organization of the human GRIK2 gene and evidence for multiple splicing variants.
Gene. 2001 Aug 22;274(1-2):187-97. doi: 10.1016/s0378-1119(01)00611-4.

本文引用的文献

4
Epigenetic Mechanisms of Longevity and Aging.长寿与衰老的表观遗传机制
Cell. 2016 Aug 11;166(4):822-839. doi: 10.1016/j.cell.2016.07.050.
7
Genome instability and aging.基因组不稳定性与衰老。
Annu Rev Physiol. 2013;75:645-68. doi: 10.1146/annurev-physiol-030212-183715.
8
Aging, cellular senescence, and cancer.衰老、细胞衰老和癌症。
Annu Rev Physiol. 2013;75:685-705. doi: 10.1146/annurev-physiol-030212-183653. Epub 2012 Nov 8.
10
Four faces of cellular senescence.细胞衰老的四个方面。
J Cell Biol. 2011 Feb 21;192(4):547-56. doi: 10.1083/jcb.201009094. Epub 2011 Feb 14.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验