Loading...
Please wait, while we are loading the content...
Similar Documents
Le rôle des microglies et de l'inflammation dans l'ischémie cérébrale
| Content Provider | Semantic Scholar |
|---|---|
| Author | Hebert, M. |
| Copyright Year | 2010 |
| Abstract | Cerebral ischemia induced acute and prolonged inflammatory response characterized by production of cytokines, infiltration of monocytes and leukocytes in the brain and activation of resident glial cells including microglia. Microglia are involved in the phagocytosis of cellular debris and production of pro-inflammatory cytokines and trophic factors. After degeneration ofthe CNS, microglial cells can play a beneficial role in cellular homeostasis and in the secretion of trophic factors. However, activation of microglial cells is also associated with the secretion of toxic molecules and attenuation of microglial activation is beneficial in some neurodegenerative disorders. In cerebral ischemia, the role of the proliferation of microglia and the dynamics of the inflammatory response remains unclear. Conditional ablation of proliferative microglial cells by the CD1 lb-TK° mouse increased the inflammatory response after cerebral ischemia and the size of the ischemic lesion. Analysis of microglial proliferative response showed that the first cells to proliferate after stroke are resident microglial cells expressing the activation marker galectin-3. After cerebral ischemia, this population serves as an endogenous pool of IGF-1, a neurotrophic molecule. The genetic inactivation of galectin-3 in mice has confirmed the beneficial role of the microglial population and the potential link between galectin 3 and induction of the mitogenic response of IGF-1. Furthermore, the longitudinal study of microglial activation using transgenic mouse TLR2-Fluc-GFP has shown that microglial activation after cerebral ischemia is biphasic and last several months after the initial attack. Two major sites of activation could be detected: the ischemic region and the olfactory bulb. Moreover, the increased signal at the site of ischemic injury is always preceded by a significant increase in TLR2 signal in the olfactory bulb. Through their special anatomical position, the microglial cells of the olfactory bulb are more sensitive to signals from the environment as much as inside the brain and may serve as sensors and / or modulators of brain inflammation. The results obtained by the analysis of different models of transgenic mice after cerebral ischemia have shown the dynamics of the inflammatory response, the neuroprotective role of microglia in proliferation and the potential link between galectin-3 and neuroprotective factor IGF-1. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://corpus.ulaval.ca/jspui/bitstream/20.500.11794/21870/1/27230.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
