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. 2020 Jul 17;72(3):1056–1072. doi: 10.1002/hep.31093

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© 2019 The Authors. Hepatology published by wiley Periodicals LLC on behalf of American Association for the study of Liver Diseases.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Silencing of HuR enhances proinflammatory signatures in BMMs. (A) Mouse (C57BL/6) BMM was subjected to LPS endotoxin for 3 hours followed by HO‐1 or HuR immunofluorescence staining. White arrows signify areas of cytoplasmic distribution. (B) Left: total lysates from LPS‐conditioned BMM were treated with siControl (siCntrl) or siHuR RNAs and probed by western blot for differences between HO‐1, HuR, and β‐Act as a loading control. Samples separated by a border were analyzed on the same western blot. Equal protein amounts (25 μg) from protein lysates were loaded on each lane. Right: quantitation of HO‐1, data shown are mean ± SEM, *P < 0.0333; siHuR +LPS versus siCntrl +LPS. (C) Inflammatory cytokine analyses of TNF‐α by qPCR. (D) mRNA coding for inflammatory chemokines (MCP1, CXCL2). Data were normalized to B2M gene expression, n = 3. Act, actin; DAPI, 4′,6‐diamidino‐2‐phenylindole.