Involvement of Mincle and Syk in the changes to innate immunity after ischemic stroke

Citations Over TimeTop 10% of 2013 papers

Abstract

Accumulating evidence shows that post-ischemic inflammation originated by Toll-like receptors (TLR) plays critical roles in ischemic stroke. However, the functions of other innate immune receptors are poorly understood in cerebral ischemia. Macrophage-inducible C-type lectin, Mincle, is one of the innate immune receptor C-type lectin-like receptor (CLR) to response against dying cells. In the present study, we showed that Mincle, its ligand SAP130, and its downstream phospho-Syk/Syk were upregulated after ischemia, and that Mincle is expressed in immune and non-immune cells in the ischemic brains of mice and human. We treated mice with piceatannol, a Syk inhibitor, and consequently the infarct volume and swelling were suppressed by piceatannol. The levels of phospho-Syk, MMP9 and ICAM-1 were downregulated, and the level of Claudin5 was uplegurated in piceatannol-treated groups. These data indicate that innate immune system, such as Mincle and Syk plays a pivotal role in the pathogenesis after the ischemia and reperfusion.

Related Papers

• → Genetic and Pharmacological Analyses of Syk Function in IIbβ3 Signaling in Platelets(1999)158 cited
• → Syk Activation Initiates Downstream Signaling Events During Human Polymorphonuclear Leukocyte Phagocytosis(1999)98 cited
• → IL-4Rα, a New Member that Associates with Syk Kinase: Implication in IL-4-Induced Human Neutrophil Functions(2009)28 cited
• → Piceatannol is an effective inhibitor of IgE‐mediated secretion from human basophils but is neither selective for this receptor nor acts on syk kinase at concentrations where mediator release inhibition occurs(2001)29 cited
• → Genetic and Pharmacological Analyses of Syk Function in IIbβ3 Signaling in Platelets(1999)17 cited