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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Book ChapterDOI
The Role of Nonneuronal Nrf2 Pathway in Ischemic Stroke: Damage Control and Potential Tissue Repair
Tuo Yang,Yang Sun,Feng Zhang +2 more
TL;DR: Nrf2 pathway is introduced, followed by its key roles of nonneuronal Nrf2 in limiting ischemic injury and emerging roles in brain tissue repair after stroke and the roles of microglias in stroke are still controversial, but close to be clarified.
Book ChapterDOI
Tissue regeneration and reprogramming
TL;DR: The current chapter addresses the role of various cells in process of regeneration and repair process and suggests a turning back of the dial of cellular plasticity in response to injury leads to acquisition of multipotency or a reversion to stem-like state in an effort to support tissue repair.
Journal ArticleDOI
Positron emission tomography of cerebral angiogenesis and TSPO expression in a mouse model of chronic hypoxia
Iwao Kanno,Chie Seki,Hiroyuki Takuwa,Zhao-Hui Jin,Didier Boturyn,Pascal Dumy,Takako Furukawa,Tsuneo Saga,Hiroshi Ito,Kazuto Masamoto,Kazuto Masamoto +10 more
TL;DR: A transient increase in TSPO probe uptake was detected with PET at only the early phase of hypoxia, which indicates an early sign of vascular remodeling induced by hypoxIA.
Journal ArticleDOI
Friends or foes: The mononuclear phagocyte system in ischemic stroke
TL;DR: In this paper , the authors reviewed articles focusing on various functions of the MPS among different phases of IS, including recruitment, polarization, phagocytosis, angiogenesis, and interaction with other types of cells.
Journal ArticleDOI
Targeting Persistent Neuroinflammation after Hypoxic-Ischemic Encephalopathy—Is Exendin-4 the Answer?
TL;DR: Preclinical and clinical studies have shown that there is still persistent neuroinflammation even after treating with therapeutic hypothermia, which may contribute to the deficits seen in infants despite treatment, which suggests that potentially targeting this persistent neuro inflammation would have an additive benefit in addition to therapeutic Hypoxic-ischemic encephalopathy.
References
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