Autocrine S100B in Astrocytes Promotes VEGF-Dependent Inflammation and Oxidative Stress, and Causes Impairment of Neuroprotection
نویسندگان
چکیده
Our previous study revealed that minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of induction inflammatory response in MHE astrocytes remains unclear. In this study, we further investigated effect and S100B, predominant isoform expressed released from mature astrocytes, on MHE-like neuropathology rat model. We discovered S100B expressions autocrine were significantly increased rats isolated rats. Furthermore, found stimulates VEGF expression via interaction between TLR2 RAGE an manner. S100B-facilitated led to a VEGFR2 COX-2 interaction, which turn induced activation NFƙB, eventually resulting inflammation oxidative stress caused by astrocytes. Compared WT impairment supported neuronal growth co-culture. To sum up, comprehensive-understanding impact S100B-overexpressed astrocyte pathology may provide insights into etiology MHE. Funding: This was Basic Scientific Research Projects Wenzhou city (Y20180076)，Natural Science Foundation Zhejiang province (LY21H030012) Natural China (81671042, 81300308). Declaration Interest: None declare. Ethical Approval: The approved Ethics Committee First Affiliated Hospital Medical University.
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ژورنال
عنوان ژورنال: Social Science Research Network
سال: 2021
ISSN: ['1556-5068']
DOI: https://doi.org/10.2139/ssrn.3817439