http://www.ncbi.nlm.nih.gov/pubmed/24256257
García-Ovejero D, Arévalo-Martín A, Navarro-Galve B, Pinteaux E, Molina-Holgado E, Molina-Holgado F.
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*Laboratory of Neuroinflammation, Unidad de Neurologia Experimental, Hospital Nacional de Parapléjicos (SESCAM), 45071 Toledo, Spain.Abstract
Neuroimmune
networks and the brain endocannabinoid system contribute to the
maintenance of neurogenesis. Activation of cannabinoid receptors
suppresses chronic inflammatory responses through the attenuation of
pro-inflammatory mediators. Moreover, the endocannabinoid system directs
cell fate specification of NSCs (neural stem cells) in the CNS (central
nervous sytem). The aim of our work is to understand better the
relationship between the endocannabinoid and the IL-1β (interleukin-1β)
associated signalling pathways and NSC biology, in order to develop
therapeutical strategies on CNS diseases that may facilitate brain
repair. NSCs express functional CB1 and CB2 cannabinoid receptors, DAGLα
(diacylglycerol lipase α) and the NSC markers SOX-2 and nestin. We have
investigated the role of CB1 and CB2 cannabinoid receptors in the
control of NSC proliferation and in the release of immunomodulators
[IL-1β and IL-1Ra (IL-1 receptor antagonist)] that control NSC fate
decisions. Pharmacological blockade of CB1 and/or CB2 cannabinoid
receptors abolish or decrease NSC proliferation, indicating a critical
role for both CB1 and CB2 receptors in the proliferation of NSC via IL-1
signalling pathways. Thus the endocannabinoid system, which has
neuroprotective and immunomodulatory actions mediated by IL-1 signalling
cascades in the brain, could assist the process of proliferation and
differentiation of embryonic or adult NSCs, and this may be of
therapeutic interest in the emerging field of brain repair.
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