Abstract:
:RNase L mediates interferon (IFN) function during viral infection and cell proliferation. Furthermore, the role of RNase L in the regulation of gene expression, cell apoptosis, autophagy, and innate immunity has been well established in the last decade. Tissue distribution reveals that RNase L is highly expressed in the lung and other organs. However, the physiological roles of RNase L in the lung are largely unknown. In this study, we found that polysaccharide (LPS)-induced acute lung injury (ALI) was remarkably intensified in mice deficient in RNase L compared to wild type mice under the same condition. Furthermore, we found that RNase L mediated the TLR4 signaling pathway, and regulated the expression of various pro- and anti-inflammatory genes in the lung tissue and blood. Most importantly, RNase L function in macrophages during LPS stimulation may be independent of the 2-5A system. These findings demonstrate a novel role of RNase L in the immune response via an atypical molecular mechanism.
journal_name
Virusesjournal_title
Virusesauthors
Wei R,Chen G,Algehainy N,Zeng C,Liu C,Liu H,Liu W,Stacey D,Zhou Adoi
10.3390/v12010073subject
Has Abstractpub_date
2020-01-07 00:00:00issue
1issn
1999-4915pii
v12010073journal_volume
12pub_type
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