Differential K + Channels Expression in “Classically” and “Alternatively” Activated Microglia
نویسندگان
چکیده
منابع مشابه
Differential Kv1.3, KCa3.1, and Kir2.1 expression in “classically” and “alternatively” activated microglia
Microglia are highly plastic cells that can assume different phenotypes in response to microenvironmental signals. Lipopolysaccharide (LPS) and interferon-γ (IFN-γ) promote differentiation into classically activated M1-like microglia, which produce high levels of pro-inflammatory cytokines and nitric oxide and are thought to contribute to neurological damage in ischemic stroke and Alzheimer's d...
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Alternatively activated macrophages (aaMphi) display molecular and biological characteristics that differ from those of classically activated macrophages (caMphi). Recently, we described an experimental model of murine trypanosomosis in which the early stage of infection of mice with a Trypanosoma brucei brucei variant is characterized by the development of caMphi, whereas in the late and chron...
متن کاملP2Y12 expression and function in alternatively activated human microglia
OBJECTIVE To investigate and measure the functional significance of altered P2Y12 expression in the context of human microglia activation. METHODS We performed in vitro and in situ experiments to measure how P2Y12 expression can influence disease-relevant functional properties of classically activated (M1) and alternatively activated (M2) human microglia in the inflamed brain. RESULTS We de...
متن کاملP2Y12 expression and function in alternatively activated human microglia
In the article " P2Y12 expression and function in alternatively activated human microglia " by C.S. Moore et al. (Neurology ® Neuroimmunology & Neuroinflammation 2015;2:e80), there is an error in figure 6, panel C, first image. The image should have been titled CD163. The editorial staff regrets the error.
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Background: Microglial activation contributes strongly to brain inflammation. Results: The modulation of microglial cyclooxygenase-2, iNOS and cytokine production by EP2 (PTGER2) activation is not blocked by a protein kinase A antagonist, but is mimicked by an Epac agonist. Conclusion: Epac signaling pathways prominently contribute to the modulation of microglial activation by EP2. Significance...
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ژورنال
عنوان ژورنال: Biophysical Journal
سال: 2017
ISSN: 0006-3495
DOI: 10.1016/j.bpj.2016.11.1805