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Endothelial TLR4 and the microbiome drive cerebral cavernous malformations.

Nature. 2017; 
Tang Alan T,Choi Jaesung P,Kotzin Jonathan J,Yang Yiqing,Hong Courtney C,Hobson Nicholas,Girard Romuald,Zeineddine Hussein A,Lightle Rhonda,Moore Thomas,Cao Ying,Shenkar Robert,Chen Mei,Mericko Patricia,Yang Jisheng,Li Li,Tanes Ceylan,Kobuley Dmytro,Võsa Urmo,Whitehead Kevin J,Li Dean Y,Franke Lude,Hart Blaine,Schwaninger Markus,Henao-Mejia Jorge,Morrison Leslie,Kim Helen,Awad Issam A,Zheng Xiangjian,Kahn Ma
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Molecular Biology Reagents Mouse IL-1β was purchased from Genscript (Z02988) and administered to the resistant Ccm2ECKO neonatal CCM disease model.... Mouse TNFα was purchased from Genscript (Z02918) and administered to the resistant Ccm2ECKO neonatal CCM disease model under identical conditions as the IL-1β experiments. Get A Quote

摘要

Cerebral cavernous malformations (CCMs) are a cause of stroke and seizure for which no effective medical therapies yet exist. CCMs arise from the loss of an adaptor complex that negatively regulates MEKK3-KLF2/4 signalling in brain endothelial cells, but upstream activators of this disease pathway have yet to be identified. Here we identify endothelial Toll-like receptor 4 (TLR4) and the gut microbiome as critical stimulants of CCM formation. Activation of TLR4 by Gram-negative bacteria or lipopolysaccharide accelerates CCM formation, and genetic or pharmacologic blockade of TLR4 signalling prevents CCM formation in mice. Polymorphisms that increase expression of the TLR4 gene or the gene encoding its co-re... More

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