The extracellular matrix controls gap junction protein expression and function in postnatal hippocampal neural progenitor cells

Persistent Link:
http://hdl.handle.net/10150/610072
Title:
The extracellular matrix controls gap junction protein expression and function in postnatal hippocampal neural progenitor cells
Author:
Imbeault, Sophie; Gauvin, Lianne; Toeg, Hadi; Pettit, Alexandra; Sorbara, Catherine; Migahed, Lamiaa; DesRoches, Rebecca; Menzies, A. S.; Nishii, Kiyomasa; Paul, David; Simon, Alexander; Bennett, Steffany
Affiliation:
Neural Regeneration Laboratory and Ottawa Institute of Systems Biology, Dept. of Biochemistry, Microbiology, and Immunology, University of Ottawa, ON, Canada; Dept. of Neurobiology, Harvard Medical School, Boston, MA, USA; Dept. of Cellular Neurobiology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; Dept. of Physiology, University of Arizona, Tucson, AZ, USA
Issue Date:
2009
Publisher:
BioMed Central
Citation:
BMC Neuroscience 2009, 10:13 doi:10.1186/1471-2202-10-13
Journal:
BMC Neuroscience
Rights:
© 2009 Imbeault et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
BACKGROUND:Gap junction protein and extracellular matrix signalling systems act in concert to influence developmental specification of neural stem and progenitor cells. It is not known how these two signalling systems interact. Here, we examined the role of ECM components in regulating connexin expression and function in postnatal hippocampal progenitor cells.RESULTS:We found that Cx26, Cx29, Cx30, Cx37, Cx40, Cx43, Cx45, and Cx47 mRNA and protein but only Cx32 and Cx36 mRNA are detected in distinct neural progenitor cell populations cultured in the absence of exogenous ECM. Multipotential Type 1 cells express Cx26, Cx30, and Cx43 protein. Their Type 2a progeny but not Type 2b and 3 neuronally committed progenitor cells additionally express Cx37, Cx40, and Cx45. Cx29 and Cx47 protein is detected in early oligodendrocyte progenitors and mature oligodendrocytes respectively. Engagement with a laminin substrate markedly increases Cx26 protein expression, decreases Cx40, Cx43, Cx45, and Cx47 protein expression, and alters subcellular localization of Cx30. These changes are associated with decreased neurogenesis. Further, laminin elicits the appearance of Cx32 protein in early oligodendrocyte progenitors and Cx36 protein in immature neurons. These changes impact upon functional connexin-mediated hemichannel activity but not gap junctional intercellular communication.CONCLUSION:Together, these findings demonstrate a new role for extracellular matrix-cell interaction, specifically laminin, in the regulation of intrinsic connexin expression and function in postnatal neural progenitor cells.
EISSN:
1471-2202
DOI:
10.1186/1471-2202-10-13
Version:
Final published version
Additional Links:
http://www.biomedcentral.com/1471-2202/10/13

Full metadata record

DC FieldValue Language
dc.contributor.authorImbeault, Sophieen
dc.contributor.authorGauvin, Lianneen
dc.contributor.authorToeg, Hadien
dc.contributor.authorPettit, Alexandraen
dc.contributor.authorSorbara, Catherineen
dc.contributor.authorMigahed, Lamiaaen
dc.contributor.authorDesRoches, Rebeccaen
dc.contributor.authorMenzies, A. S.en
dc.contributor.authorNishii, Kiyomasaen
dc.contributor.authorPaul, Daviden
dc.contributor.authorSimon, Alexanderen
dc.contributor.authorBennett, Steffanyen
dc.date.accessioned2016-05-20T08:57:56Z-
dc.date.available2016-05-20T08:57:56Z-
dc.date.issued2009en
dc.identifier.citationBMC Neuroscience 2009, 10:13 doi:10.1186/1471-2202-10-13en
dc.identifier.doi10.1186/1471-2202-10-13en
dc.identifier.urihttp://hdl.handle.net/10150/610072-
dc.description.abstractBACKGROUND:Gap junction protein and extracellular matrix signalling systems act in concert to influence developmental specification of neural stem and progenitor cells. It is not known how these two signalling systems interact. Here, we examined the role of ECM components in regulating connexin expression and function in postnatal hippocampal progenitor cells.RESULTS:We found that Cx26, Cx29, Cx30, Cx37, Cx40, Cx43, Cx45, and Cx47 mRNA and protein but only Cx32 and Cx36 mRNA are detected in distinct neural progenitor cell populations cultured in the absence of exogenous ECM. Multipotential Type 1 cells express Cx26, Cx30, and Cx43 protein. Their Type 2a progeny but not Type 2b and 3 neuronally committed progenitor cells additionally express Cx37, Cx40, and Cx45. Cx29 and Cx47 protein is detected in early oligodendrocyte progenitors and mature oligodendrocytes respectively. Engagement with a laminin substrate markedly increases Cx26 protein expression, decreases Cx40, Cx43, Cx45, and Cx47 protein expression, and alters subcellular localization of Cx30. These changes are associated with decreased neurogenesis. Further, laminin elicits the appearance of Cx32 protein in early oligodendrocyte progenitors and Cx36 protein in immature neurons. These changes impact upon functional connexin-mediated hemichannel activity but not gap junctional intercellular communication.CONCLUSION:Together, these findings demonstrate a new role for extracellular matrix-cell interaction, specifically laminin, in the regulation of intrinsic connexin expression and function in postnatal neural progenitor cells.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.biomedcentral.com/1471-2202/10/13en
dc.rights© 2009 Imbeault et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)en
dc.titleThe extracellular matrix controls gap junction protein expression and function in postnatal hippocampal neural progenitor cellsen
dc.typeArticleen
dc.identifier.eissn1471-2202en
dc.contributor.departmentNeural Regeneration Laboratory and Ottawa Institute of Systems Biology, Dept. of Biochemistry, Microbiology, and Immunology, University of Ottawa, ON, Canadaen
dc.contributor.departmentDept. of Neurobiology, Harvard Medical School, Boston, MA, USAen
dc.contributor.departmentDept. of Cellular Neurobiology, Graduate School of Medicine, University of Tokyo, Tokyo, Japanen
dc.contributor.departmentDept. of Physiology, University of Arizona, Tucson, AZ, USAen
dc.identifier.journalBMC Neuroscienceen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
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