GST/MCP-1 fusion protein was overexpressed in Escherichia coli as inculstion bodies. After isolation of the inclusion bodies, the optimum conditions of denaturation and renaturation were studied. The renatured produts were purified to be electroporetically pure by affinity chromatography on immobilised glutathione. The purified product remains biological activities and can react specifically with MCP-1 antibodies by western blot analysis. The in vitro antitumor effect showed that GST/MCP-1 could activate monocytes and lymphocytes to inhibit the growth of a lung adenocarcinoma cell line A549. In vivo, GST/MCP-1 could inhibit the tumor growth in nude mice. These results suggested that MCP-1 had antitumor effect.

The brain pericyte is a unique and indispensable part of the blood-brain barrier (BBB), and contributes to several pathological processes in traumatic brain injury (TBI). However, the cellular and molecular mechanisms by which pericytes are regulated in the damaged brain are largely unknown. Here, we show that the formation of neutrophil extracellular traps (NETs) induces the appearance of CD11b⁺ pericytes after TBI. These CD11b⁺ pericyte subsets are characterized by increased permeability and pro-inflammatory profiles compared to CD11b^- pericytes. Moreover, histones from NETs by Dectin-1 facilitate CD11b induction in brain pericytes in PKC-c-Jun dependent manner, resulting in neuroinflammation and BBB dysfunction after TBI. These data indicate that neutrophil-NET-pericyte and histone-Dectin-1-CD11b are possible mechanisms for the activation and dysfunction of pericytes. Targeting NETs formation and Dectin-1 are promising means of treating TBI.
Blood-Brain Barrier/metabolism* ; Brain/pathology* ; Brain Injuries, Traumatic/metabolism* ; Extracellular Traps/metabolism* ; Histones ; Humans ; Lectins, C-Type ; Pericytes/pathology*