The ischemic environment drives microglia and macrophage function.
Stefano Fumagalli,Stefano Fumagalli,Carlo Perego,Francesca Pischiutta,Elisa R. Zanier,Maria Grazia De Simoni +5 more
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TLDR
The selective responses of microglia and macrophages to hypoxia after stroke are discussed and relevant markers are reviewed with the aim of defining the different subpopulations of myeloid cells that are recruited to the injured site.Abstract:
Cells of myeloid origin, such as microglia and macrophages, act at the crossroads of several inflammatory mechanisms during pathophysiology. Besides pro-inflammatory activity (M1 polarization), myeloid cells acquire protective functions (M2) and participate in the neuroprotective innate mechanisms after brain injury. Experimental research is making considerable efforts to understand the rules that regulate the balance between toxic and protective brain innate immunity. Environmental changes affect microglia/macrophage functions. Hypoxia can affect myeloid cell distribution, activity, and phenotype. With their intrinsic differences, microglia and macrophages respond differently to hypoxia, the former depending on ATP to activate and the latter switching to anaerobic metabolism and adapting to hypoxia. Myeloid cell functions include homeostasis control, damage-sensing activity, chemotaxis, and phagocytosis, all distinctive features of these cells. Specific markers and morphologies enable to recognize each functional state. To ensure homeostasis and activate when needed, microglia/macrophage physiology is finely tuned. Microglia are controlled by several neuron-derived components, including contact-dependent inhibitory signals and soluble molecules. Changes in this control can cause chronic activation or priming with specific functional consequences. Strategies, such as stem cell treatment, may enhance microglia protective polarization. This review presents data from the literature that has greatly advanced our understanding of myeloid cell action in brain injury. We discuss the selective responses of microglia and macrophages to hypoxia after stroke and review relevant markers with the aim of defining the different subpopulations of myeloid cells that are recruited to the injured site. We also cover the functional consequences of chronically active microglia and review pivotal works on microglia regulation that offer new therapeutic possibilities for acute brain injury.read more
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Differential gene expression in the contralateral hemisphere of the rat brain after focal ischemia
Ivan B. Filippenkov,Julia A Remizova,Alina E. Denisova,Vasily V. Stavchansky,Ksenia D Golovina,Leonid V. Gubsky,Svetlana A. Limborska,Lyudmila V. Dergunova +7 more
TL;DR: In this paper , the authors performed functional genetic analysis of the processes occurring in the contralateral hemisphere (CH) after ischemia-reperfusion injury in rat brain.
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Dynamics of Microglia Activation in the Ischemic Brain: Implications for Myelin Repair and Functional Recovery
Stefano Raffaele,Marta Fumagalli +1 more
TL;DR: Recent evidence describing microglia activation kinetics in experimental models of ischemic injury is summarized, focusing on the contribution of these innate immune cells to myelin damage and repair.
Journal ArticleDOI
Phagocytosis converts infiltrated monocytes to microglia-like phenotype in experimental brain ischemia
TL;DR: In this article , the authors defined the origin and function of macrophages in cerebral ischemia and demonstrated that MDMs are the predominant phagocytes in the post-ischemic brain, with the CD45 High subset having the highest phagocytic activity levels.
Journal ArticleDOI
Changes in arginase isoforms in a murine model of neonatal brain hypoxia-ischemia.
TL;DR: ARG isoform expression increases with age from P9 to P17, but is suppressed by injury specifically in the hippocampus and not in the cortex, while ARG-1 immunolabelling is upregulated in the HI cortex.
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