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dc.contributor.author
Belkacemi, Thabet
dc.contributor.author
Niermann, Alexander
dc.contributor.author
Hofmann, Laura
dc.contributor.author
Wissenbach, Ulrich
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Birnbaumer, Lutz
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Leidinger, Petra
dc.contributor.author
Backes, Christina
dc.contributor.author
Meese, Eckart
dc.contributor.author
Keller, Andreas
dc.contributor.author
Bai, Xianshu
dc.contributor.author
Scheller, Anja
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Kirchhoff, Frank
dc.contributor.author
Philipp, Stephan E.
dc.contributor.author
Weissgerber, Petra
dc.contributor.author
Flockerzi, Veit
dc.contributor.author
Beck, Andreas
dc.date.available
2018-06-25T17:27:17Z
dc.date.issued
2017-06
dc.identifier.citation
Belkacemi, Thabet; Niermann, Alexander; Hofmann, Laura; Wissenbach, Ulrich; Birnbaumer, Lutz; et al.; TRPC1- and TRPC3-dependent Ca2+ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo; Wiley-liss, Div John Wiley & Sons Inc; Glia; 65; 9; 6-2017; 1535-1549
dc.identifier.issn
0894-1491
dc.identifier.uri
http://hdl.handle.net/11336/49949
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Wiley-liss, Div John Wiley & Sons Inc
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Glia
dc.subject
Ion Channels
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Membrane Currents
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Migration
dc.subject
Proliferation
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Stab Wound Injury
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Inmunología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
TRPC1- and TRPC3-dependent Ca2+ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-06-07T14:22:27Z
dc.identifier.eissn
1098-1136
dc.journal.volume
65
dc.journal.number
9
dc.journal.pagination
1535-1549
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Belkacemi, Thabet. Universitat Saarland; Alemania
dc.description.fil
Fil: Niermann, Alexander. Universitat Saarland; Alemania
dc.description.fil
Fil: Hofmann, Laura. Universitat Saarland; Alemania
dc.description.fil
Fil: Wissenbach, Ulrich. Universitat Saarland; Alemania
dc.description.fil
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina ; Argentina. National Institute of Environmental Health Sciences; Estados Unidos
dc.description.fil
Fil: Leidinger, Petra. Universitat Saarland; Alemania
dc.description.fil
Fil: Backes, Christina. Universitat Saarland; Alemania
dc.description.fil
Fil: Meese, Eckart. Universitat Saarland; Alemania
dc.description.fil
Fil: Keller, Andreas. Universitat Saarland; Alemania
dc.description.fil
Fil: Bai, Xianshu. Universitat Saarland; Alemania
dc.description.fil
Fil: Scheller, Anja. Universitat Saarland; Alemania
dc.description.fil
Fil: Kirchhoff, Frank. Universitat Saarland; Alemania
dc.description.fil
Fil: Philipp, Stephan E.. Universitat Saarland; Alemania
dc.description.fil
Fil: Weissgerber, Petra. Universitat Saarland; Alemania
dc.description.fil
Fil: Flockerzi, Veit. Universitat Saarland; Alemania
dc.description.fil
Fil: Beck, Andreas. Universitat Saarland; Alemania
dc.journal.title
Glia
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1002/glia.23180
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/glia.23180
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