FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2402129233> ?p ?o ?g. }

• W2402129233 endingPage "e1002466" @default.
• W2402129233 startingPage "e1002466" @default.
• W2402129233 abstract "Phagocytosis is essential to maintain tissue homeostasis in a large number of inflammatory and autoimmune diseases, but its role in the diseased brain is poorly explored. Recent findings suggest that in the adult hippocampal neurogenic niche, where the excess of newborn cells undergo apoptosis in physiological conditions, phagocytosis is efficiently executed by surveillant, ramified microglia. To test whether microglia are efficient phagocytes in the diseased brain as well, we confronted them with a series of apoptotic challenges and discovered a generalized response. When challenged with excitotoxicity in vitro (via the glutamate agonist NMDA) or inflammation in vivo (via systemic administration of bacterial lipopolysaccharides or by omega 3 fatty acid deficient diets), microglia resorted to different strategies to boost their phagocytic efficiency and compensate for the increased number of apoptotic cells, thus maintaining phagocytosis and apoptosis tightly coupled. Unexpectedly, this coupling was chronically lost in a mouse model of mesial temporal lobe epilepsy (MTLE) as well as in hippocampal tissue resected from individuals with MTLE, a major neurological disorder characterized by seizures, excitotoxicity, and inflammation. Importantly, the loss of phagocytosis/apoptosis coupling correlated with the expression of microglial proinflammatory, epileptogenic cytokines, suggesting its contribution to the pathophysiology of epilepsy. The phagocytic blockade resulted from reduced microglial surveillance and apoptotic cell recognition receptor expression and was not directly mediated by signaling through microglial glutamate receptors. Instead, it was related to the disruption of local ATP microgradients caused by the hyperactivity of the hippocampal network, at least in the acute phase of epilepsy. Finally, the uncoupling led to an accumulation of apoptotic newborn cells in the neurogenic niche that was due not to decreased survival but to delayed cell clearance after seizures. These results demonstrate that the efficiency of microglial phagocytosis critically affects the dynamics of apoptosis and urge to routinely assess the microglial phagocytic efficiency in neurodegenerative disorders." @default.
• W2402129233 created "2016-06-24" @default.
• W2402129233 creator A5003131263 @default.
• W2402129233 creator A5006668325 @default.
• W2402129233 creator A5008266377 @default.
• W2402129233 creator A5013908994 @default.
• W2402129233 creator A5021223799 @default.
• W2402129233 creator A5022531075 @default.
• W2402129233 creator A5032421860 @default.
• W2402129233 creator A5034941660 @default.
• W2402129233 creator A5036133419 @default.
• W2402129233 creator A5037399867 @default.
• W2402129233 creator A5038221893 @default.
• W2402129233 creator A5038886759 @default.
• W2402129233 creator A5041308096 @default.
• W2402129233 creator A5041638964 @default.
• W2402129233 creator A5050200659 @default.
• W2402129233 creator A5054534155 @default.
• W2402129233 creator A5057086204 @default.
• W2402129233 creator A5061659832 @default.
• W2402129233 creator A5062064926 @default.
• W2402129233 creator A5066339227 @default.
• W2402129233 creator A5069937879 @default.
• W2402129233 creator A5073129412 @default.
• W2402129233 creator A5074921706 @default.
• W2402129233 creator A5078083717 @default.
• W2402129233 creator A5087618643 @default.
• W2402129233 creator A5091309671 @default.
• W2402129233 date "2016-05-26" @default.
• W2402129233 modified "2023-10-18" @default.
• W2402129233 title "Neuronal Hyperactivity Disturbs ATP Microgradients, Impairs Microglial Motility, and Reduces Phagocytic Receptor Expression Triggering Apoptosis/Microglial Phagocytosis Uncoupling" @default.
• W2402129233 cites W1480157650 @default.
• W2402129233 cites W1482674003 @default.
• W2402129233 cites W1563061718 @default.
• W2402129233 cites W1595975262 @default.
• W2402129233 cites W1619824188 @default.
• W2402129233 cites W1879709537 @default.
• W2402129233 cites W1942784841 @default.
• W2402129233 cites W1958394803 @default.
• W2402129233 cites W1963696719 @default.
• W2402129233 cites W1963872045 @default.
• W2402129233 cites W1964600153 @default.
• W2402129233 cites W1964713902 @default.
• W2402129233 cites W1965130745 @default.
• W2402129233 cites W1971084572 @default.
• W2402129233 cites W1971959365 @default.
• W2402129233 cites W1979286651 @default.
• W2402129233 cites W1983949013 @default.
• W2402129233 cites W1985473475 @default.
• W2402129233 cites W1989991560 @default.
• W2402129233 cites W1990161015 @default.
• W2402129233 cites W1994909588 @default.
• W2402129233 cites W1997602206 @default.
• W2402129233 cites W1997795701 @default.
• W2402129233 cites W2001004870 @default.
• W2402129233 cites W2005198093 @default.
• W2402129233 cites W2007055364 @default.
• W2402129233 cites W2008639289 @default.
• W2402129233 cites W2011221727 @default.
• W2402129233 cites W2011580597 @default.
• W2402129233 cites W2012624148 @default.
• W2402129233 cites W2014190388 @default.
• W2402129233 cites W2022981588 @default.
• W2402129233 cites W2027467386 @default.
• W2402129233 cites W2028167589 @default.
• W2402129233 cites W2029826677 @default.
• W2402129233 cites W2034101077 @default.
• W2402129233 cites W2044110964 @default.
• W2402129233 cites W2045828483 @default.
• W2402129233 cites W2050016412 @default.
• W2402129233 cites W2051639780 @default.
• W2402129233 cites W2054552572 @default.
• W2402129233 cites W2057310829 @default.
• W2402129233 cites W2058263100 @default.
• W2402129233 cites W2058478749 @default.
• W2402129233 cites W2061657865 @default.
• W2402129233 cites W2066943555 @default.
• W2402129233 cites W2071420776 @default.
• W2402129233 cites W2074661552 @default.
• W2402129233 cites W2079981730 @default.
• W2402129233 cites W2081250995 @default.
• W2402129233 cites W2085429387 @default.
• W2402129233 cites W2088494800 @default.
• W2402129233 cites W2090012338 @default.
• W2402129233 cites W2091493364 @default.
• W2402129233 cites W2094660330 @default.
• W2402129233 cites W2098569132 @default.
• W2402129233 cites W2100343757 @default.
• W2402129233 cites W2101853437 @default.
• W2402129233 cites W2103200506 @default.
• W2402129233 cites W2103946141 @default.
• W2402129233 cites W2110877402 @default.
• W2402129233 cites W2119958966 @default.
• W2402129233 cites W2122828560 @default.
• W2402129233 cites W2123882810 @default.
• W2402129233 cites W2130755020 @default.
• W2402129233 cites W2131686384 @default.
• W2402129233 cites W2131938193 @default.

• next