Show simple item record

dc.contributor.authorGeribaldi-Doldán, Noelia
dc.contributor.authorGómez-Oliva, Ricardo
dc.contributor.authorDomínguez-García, Samuel
dc.contributor.authorNunez-Abades, Pedro
dc.contributor.authorCastro, Carmen
dc.contributor.otherBioquímica y Biología Molecular, Microbiología, Medicina Preventiva, Salud Públicaen_US
dc.date.accessioned2019-05-23T08:36:42Z
dc.date.available2019-05-23T08:36:42Z
dc.date.issued2019-03
dc.identifier.issn2296-634X
dc.identifier.urihttp://hdl.handle.net/10498/21319
dc.description.abstractAcute or chronic injury to the central nervous system (CNS), causes neuronal death and irreversible cognitive deficits or sensory-motor alteration. Despite the capacity of the adult CNS to generate new neurons from neural stem cells (NSC), neuronal replacement following an injury is a restricted process, which does not naturally result in functional regeneration. Therefore, potentiating endogenous neurogenesis is one of the strategies that are currently being under study to regenerate damaged brain tissue. The insignificant neurogenesis that occurs in CNS injuries is a consequence of the gliogenic/non-neurogenic environment that inflammatory signaling molecules create within the injured area. The modification of the extracellular signals to generate a neurogenic environment would facilitate neuronal replacement. However, in order to generate this environment, it is necessary to unearth which molecules promote or impair neurogenesis to introduce the first and/or eliminate the latter. Specific isozymes of the protein kinase C (PKC) family differentially contribute to generate a gliogenic or neurogenic environment in injuries by regulating the ADAM17 mediated release of growth factor receptor ligands. Recent reports describe several non-tumorigenic diterpenes isolated from plants of the Euphorbia genus, which specifically modulate the activity of PKC isozymes promoting neurogenesis. Diterpenes with 12-deoxyphorbol or lathyrane skeleton, increase NPC proliferation in neurogenic niches in the adult mouse brain in a PKCb dependent manner exerting their effects on transit amplifying cells, whereas PKC inhibition in injuries promotes neurogenesis. Thus, compounds that balance PKC activity in injuries might be of use in the development of new drugs and therapeutic strategies to regenerate brain injuries.en_US
dc.formatapplication/pdfen_US
dc.language.isoengen_US
dc.publisherFRONTIERS MEDIA SAen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.sourceFrontiers in Cell and Developmental Biology - 2019 Volumen: 7 :39en_US
dc.subjectprotein kinase Cen_US
dc.subjectneurogenesisen_US
dc.subjectADAM17/TACEen_US
dc.subjectbrain injuryen_US
dc.subjectneuroregenerationen_US
dc.titleProtein Kinase C: Targets to Regenerate Brain Injuries?en_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen_US
dc.identifier.doi10.3389/fcell.2019.00039


Files in this item

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivatives 4.0 Internacional
This work is under a Creative Commons License Attribution-NonCommercial-NoDerivatives 4.0 Internacional