Inhibition of histone deacetylase reduces lipopolysaccharide-induced-inflammation in primary mammary epithelial cells by regulating ROS-NF-кB signaling pathways

Inhibition of histone deacetylase reduces lipopolysaccharide-induced-inflammation in primary... Histone deacetylase 6 (HDAC6) is the sole member of the HDAC family, that is predominantly located in the cytoplasm and has substrate specificity for nonhistone proteins, such as α-Tubulin. Although an increasing number of studies have shown that HDAC6 is involved in inflammatory diseases, but little is known about the participation of HDAC6 in the transcriptional regulation of inflammatory cytokines. Here, we examined the effects of Tubastatin (Tub), a highly selective HDAC6 inhibitor, on lipopolysaccharide (LPS)-stimulated primary bovine mammary epithelial cells (bMECs). The specific inhibition of HDAC6 using Tub significantly decreased the release of pro-inflammatory cytokines, such as TNF-α and IL-1β, which was associated with increased α-Tubulin acetylation. HDAC6 overexpression significantly induced reactive oxygen species (ROS) generation via upregulation of NADPH oxidase activity. Administration of Tub dose-dependently inhibited ROS production and NADPH oxidase activity. In addition, inhibition of HDAC6 led to suppression of the NF-κB signaling pathway. Thus, we report herein that HDAC6 is involved in ROS-NF-κB signaling pathway related to pro-inflammatory cytokine expression and that selective HDAC6 inhibition by Tub is a potent approach for preventing LPS-mediated inflammation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Immunopharmacology Elsevier

Inhibition of histone deacetylase reduces lipopolysaccharide-induced-inflammation in primary mammary epithelial cells by regulating ROS-NF-кB signaling pathways

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Publisher
Elsevier
Copyright
Copyright © 2018 Elsevier Ltd
ISSN
1567-5769
eISSN
1878-1705
D.O.I.
10.1016/j.intimp.2018.01.039
Publisher site
See Article on Publisher Site

Abstract

Histone deacetylase 6 (HDAC6) is the sole member of the HDAC family, that is predominantly located in the cytoplasm and has substrate specificity for nonhistone proteins, such as α-Tubulin. Although an increasing number of studies have shown that HDAC6 is involved in inflammatory diseases, but little is known about the participation of HDAC6 in the transcriptional regulation of inflammatory cytokines. Here, we examined the effects of Tubastatin (Tub), a highly selective HDAC6 inhibitor, on lipopolysaccharide (LPS)-stimulated primary bovine mammary epithelial cells (bMECs). The specific inhibition of HDAC6 using Tub significantly decreased the release of pro-inflammatory cytokines, such as TNF-α and IL-1β, which was associated with increased α-Tubulin acetylation. HDAC6 overexpression significantly induced reactive oxygen species (ROS) generation via upregulation of NADPH oxidase activity. Administration of Tub dose-dependently inhibited ROS production and NADPH oxidase activity. In addition, inhibition of HDAC6 led to suppression of the NF-κB signaling pathway. Thus, we report herein that HDAC6 is involved in ROS-NF-κB signaling pathway related to pro-inflammatory cytokine expression and that selective HDAC6 inhibition by Tub is a potent approach for preventing LPS-mediated inflammation.

Journal

International ImmunopharmacologyElsevier

Published: Mar 1, 2018

References

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