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

Loading next page...
 
/lp/elsevier/inhibition-of-histone-deacetylase-reduces-lipopolysaccharide-induced-9q0LIDTogY
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

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create lists to
organize your research

Export lists, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off