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DOI | 10.1002/glia.23180 |
TRPC1-and TRPC3-dependent Ca2+ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo | |
Belkacemi, Thabet1; Niermann, Alexander1; Hofmann, Laura1; Wissenbach, Ulrich1; Birnbaumer, Lutz2,3; Leidinger, Petra4; Backes, Christina5; Meese, Eckart4; Keller, Andreas5; Bai, Xianshu6; Scheller, Anja6; Kirchhoff, Frank6; Philipp, Stephan E.1; Weissgerber, Petra1; Flockerzi, Veit1; Beck, Andreas1,7 | |
发表日期 | 2017-09-01 |
ISSN | 0894-1491 |
卷号 | 65期号:9页码:1535-1549 |
英文摘要 | Following brain injury astrocytes change into a reactive state, proliferate and grow into the site of lesion, a process called astrogliosis, initiated and regulated by changes in cytoplasmic Ca2+. Transient receptor potential canonical (TRPC) channels may contribute to Ca2+ influx but their presence and possible function in astrocytes is not known. By RT-PCR and RNA sequencing we identified transcripts of Trpc1, Trpc2, Trpc3, and Trpc4 in FACS-sorted glutamate aspartate transporter (GLAST)-positive cultured mouse cortical astrocytes and subcloned full-length Trpc1 and Trpc3 cDNAs from these cells. Ca2+ entry in cortical astrocytes depended on TRPC3 and was increased in the absence of Trpc1. After co-expression of Trpc1 and Trpc3 in HEK-293 cells both proteins co-immunoprecipitate and form functional heteromeric channels, with TRPC1 reducing TRPC3 activity. In vitro, lack of Trpc3 reduced astrocyte proliferation and migration whereas the TRPC3 gain-of-function moonwalker mutation and Trpc1 deficiency increased astrocyte migration. In vivo, astrogliosis and cortex edema following stab wound injury were reduced in Trpc3(-/-) but increased in Trpc1(-/-) mice. In summary, our results show a decisive contribution of TRPC3 to astrocyte Ca2+ signaling, which is even augmented in the absence of Trpc1, in particular following brain injury. Targeted therapies to reduce TRPC3 channel activity in astrocytes might therefore be beneficial in traumatic brain injury. |
英文关键词 | glia;ion channels;membrane currents;migration;proliferation;stab wound injury |
语种 | 英语 |
WOS记录号 | WOS:000405476300010 |
来源期刊 | GLIA |
来源机构 | 美国环保署 |
文献类型 | 期刊论文 |
条目标识符 | http://gcip.llas.ac.cn/handle/2XKMVOVA/60986 |
作者单位 | 1.Expt & Klin Pharmakol & Toxikol, D-66421 Homburg, Germany; 2.Natl Inst Environm Hlth Sci, Neurobiol Lab, Res Triangle Pk, NC 27709 USA; 3.Catholic Univ Argentina, Inst Biomed Res BIOMED, C1107AFF, Buenos Aires, DF, Argentina; 4.Inst Human Genet & Anthropol, D-66421 Homburg, Germany; 5.Univ Saarland, Klin Bioinformat, D-66123 Saarbrucken, Germany; 6.Univ Saarland, Mol Physiol, D-66421 Homburg, Germany; 7.Zentrum Human & Mol Biol, D-66421 Homburg, Germany |
推荐引用方式 GB/T 7714 | Belkacemi, Thabet,Niermann, Alexander,Hofmann, Laura,et al. TRPC1-and TRPC3-dependent Ca2+ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo[J]. 美国环保署,2017,65(9):1535-1549. |
APA | Belkacemi, Thabet.,Niermann, Alexander.,Hofmann, Laura.,Wissenbach, Ulrich.,Birnbaumer, Lutz.,...&Beck, Andreas.(2017).TRPC1-and TRPC3-dependent Ca2+ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo.GLIA,65(9),1535-1549. |
MLA | Belkacemi, Thabet,et al."TRPC1-and TRPC3-dependent Ca2+ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo".GLIA 65.9(2017):1535-1549. |
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