@article{ref1,
title="Mer regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following traumatic brain injury",
journal="Journal of neuroinflammation",
year="2021",
author="Guo, Xinying and Wang, Xiaoyu and Mei, Shuhao and Lu, Jianan and Fang, Yuanjian and Xu, Shenbin and Zheng, Jingwei and Wu, Haijian and Zhang, Jianmin and Zhao, Zhen and Wang, Yirong and Shi, Ligen and Shao, Anwen and Zeng, Jianxiong and Wu, Yingxi",
volume="18",
number="1",
pages="e2-e2",
abstract="BACKGROUND: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Microglial/macrophage activation and neuroinflammation are key cellular  events following TBI, but the regulatory and functional mechanisms are still not  well understood. Myeloid-epithelial-reproductive tyrosine kinase (Mer), a member of  the Tyro-Axl-Mer (TAM) family of receptor tyrosine kinases, regulates multiple  features of microglial/macrophage physiology. However, its function in regulating  the innate immune response and microglial/macrophage M1/M2 polarization in TBI has  not been addressed. The present study aimed to evaluate the role of Mer in  regulating microglial/macrophage M1/M2 polarization and neuroinflammation following  TBI. <br><br>METHODS: The controlled cortical impact (CCI) mouse model was employed. Mer  siRNA was intracerebroventricularly administered, and recombinant protein S (PS) was  intravenously applied for intervention. The neurobehavioral assessments, RT-PCR,  Western blot, magnetic-activated cell sorting, immunohistochemistry and confocal  microscopy analysis, Nissl and Fluoro-Jade B staining, brain water content  measurement, and contusion volume assessment were performed. <br><br>RESULTS: Mer is  upregulated and regulates microglial/macrophage M1/M2 polarization and  neuroinflammation in the acute stage of TBI. Mechanistically, Mer activates the  signal transducer and activator of transcription 1 (STAT1)/suppressor of cytokine  signaling 1/3 (SOCS1/3) pathway. Inhibition of Mer markedly decreases  microglial/macrophage M2-like polarization while increases M1-like polarization,  which exacerbates the secondary brain damage and sensorimotor deficits after TBI. Recombinant PS exerts beneficial effects in TBI mice through Mer activation. <br><br>CONCLUSIONS: Mer is an important regulator of microglial/macrophage M1/M2  polarization and neuroinflammation, and may be considered as a potential target for  therapeutic intervention in TBI.<p /> <p>Language: en</p>",
language="en",
issn="1742-2094",
doi="10.1186/s12974-020-02041-7",
url="http://dx.doi.org/10.1186/s12974-020-02041-7"
}