Inflammation, plasticity and real-time imaging after cerebral ischemia.
With an incidence of approximately 350 in 100,000, stroke is the third leading cause of death and a major cause of disability in industrialized countries. At present, although progress has been made in understanding the molecular pathways that lead to ischemic cell death, the current clinical treatments remain poorly effective. There is mounting evidence that inflammation plays an important role in cerebral ischemia. Experimentally and clinically, brain response to ischemic injury is associated with an acute and prolonged inflammatory process characterized by the activation of resident glial cells, production of inflammatory cytokines as well as leukocyte and monocyte infiltration in the brain, events that may contribute to ischemic brain injury and affect brain recovery and plasticity. However, whether the post-ischemic inflammatory response is deleterious or beneficial to brain recovery is presently a matter of debate and controversies. Here, we summarize the current knowledge on the molecular mechanisms underlying post-ischemic neuronal plasticity and the potential role of inflammation in regenerative processes and functional recovery after stroke. Furthermore, because of the dynamic nature of the brain inflammatory response, we highlight the importance of the development of novel experimental approaches such as real-time imaging. Finally, we discuss the novel transgenic reporter mice models that have allowed us to visualize and to analyze the processes such as neuroinflammation and neuronal repair from the ischemic brains of live animals.
Kriz
Jasna
J
Department of Anatomy and Physiology, Faculty of Medicine, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUQ), T3-67, Laval University, 2705 Boulevard Laurier, Quebec, QC, G1V 4G2, Canada. Jasna.Kriz@crchul.ulaval.ca
Lalancette-Hébert
Mélanie
M
D000818:Animals; D015374:Biosensing Techniques / Q000379:methods; D001921:Brain / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D002545:Brain Ischemia / Q000175:diagnosis* / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D049452:Green Fluorescent Proteins; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D008156:Luciferases; D051379:Mice; D008822:Mice, Transgenic; D009457:Neuroglia / Q000276:immunology*; D009473:Neuronal Plasticity; D020127:Recovery of Function; D013997:Time Factors; D051195:Toll-Like Receptor 2 / Q000378:metabolism
D016207:Cytokines; D051195:Toll-Like Receptor 2; D049452:Green Fluorescent Proteins; D008156:Luciferases