NDLI: Oxidative stress and TNF-α induce histone acetylation and NF-κB/AP-1 activation in alveolar epithelial cells: Potential mechanism in gene transcription in lung inflammation

Content Provider	SpringerLink
Author	Rahman, Irfan Gilmour, Peter S. Jimenez, Luis Albert MacNee, William
Copyright Year	2002
Abstract	Oxidants and inflammatory mediators such as tumour necrosis factor-α (TNF-α) activate nuclear factor kappa B (NF-κB) and activator protein-1 (AP-1) transcription factors, and enhance the expression of both pro-inflammatory and protective antioxidant genes. Remodelling of chromatin within the nucleus, controlled by the degree of acetylation/deacetylation of histone residues on the histone core around which DNA is coiled, is important in allowing access for transcription factor DNA binding and hence gene transcription. Unwinding of DNA is important in allowing access for transcription factor DNA binding and hence gene transcription. Nuclear histone acetylation is a reversible process, and is regulated by a group of acetyltransferases (HATs) which promote acetylation, and deacetylases (HDACs) which promote deacetylation. The aim of this study was to determine whether oxidative stress and the pro-inflammatory mediator, TNF-α, altered histone acetylation/deacetylation and the activation of NF-κB and AP-1, leading to the release of the pro-inflammatory cytokine IL-8 in human alveolar epithelial cells (A549). Hydrogen peroxide (H$_{2}$O$_{2}$) (100 μM) and TNF-α (10 ng/ml) imposed oxidative stress in A549 cells as shown by depletion of the antioxidant reduced glutathione (GSH) concomitant with increased levels of oxidised glutathione (GSSG). Treatment of A549 cells with H$_{2}$O$_{2}$, TNF-α and the HDAC inhibitor, trichostatin A, TSA (100 ng/ml) significantly increased acetylation of histone proteins shown by immunostaining of cells and increased HAT activity, compared to the untreated cells. H$_{2}$O$_{2}$, and TNF-α, and TSA all increased NF-κB and AP-1 DNA binding to their consensus sites assessed by the electrophoretic mobility shift assay. TSA treatment potentiated the increased AP-1 and NF-κB binding, produced by H$_{2}$O$_{2}$ or TNF-α treatments in A549 cells. Both H$_{2}$O$_{2}$ and TNF-α significantly increased IL-8 release, which was further enhanced by pre-treatment of A549 cells with TSA compared to the individual treatments. This study shows that the oxidant H$_{2}$O$_{2}$ and the pro-inflammatory mediator, TNF-α induce histone acetylation which is associated with decreased GSH levels and increased AP-1 and NF-κB activation leading to enhanced proinflammatory IL-8 release in alveolar epithelial cells. This indicates a mechanism for the pro-inflammatory effects of oxidative stress.
Starting Page	239
Ending Page	248
Page Count	10
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	234
Issue Number	1
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2002-01-01
Publisher Place	Boston
Access Restriction	Subscribed
Subject Keyword	Cardiology Medical Biochemistry Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Clinical Biochemistry Cell Biology Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Libarray of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Dihydromyricetin suppresses TNF-α-induced NF-κB activation and target gene expression

IL-1 promotes α-epithelial Sodium Channel (α-ENaC) expression in murine lung epithelial cells: involvement of NF-κB.

Protein Kinase Cζ Mediates Cigarette Smoke/Aldehyde- and Lipopolysaccharide-induced Lung Inflammation and Histone Modifications

Diesel Exhaust Particles Induce the Over expression of Tumor Necrosis Factor-α (TNF-α) Gene in Alveolar Macrophages and Failed to Induce Apoptosis through Activation of Nuclear Factor-κB (NF-κB)

Astragalus membranaceus Extract Attenuates Inflammation and Oxidative Stress in Intestinal Epithelial Cells via NF-κB Activation and Nrf2 Response

TNF Receptor-Associated Factor-2 Is Involved in Both IL-1β and TNF-α Signaling Cascades Leading to NF-κB Activation and IL-8 Expression in Human Intestinal Epithelial Cells

Multiwalled carbon nanotubes activate NF-κB and AP-1 signaling pathways to induce apoptosis in rat lung epithelial cells

Luteolin suppresses inflammation-associated gene expression by blocking NF-kappaB and AP-1 activation pathway in mouse alveolar macrophages.

HPV16 E2-mediated potentiation of NF-κB activation induced by TNF-α involves parallel activation of STAT3 with a reduction in E2-induced apoptosis

Oxidative stress and TNF-α induce histone acetylation and NF-κB/AP-1 activation in alveolar epithelial cells: Potential mechanism in gene transcription in lung inflammation

Similar Documents

Dihydromyricetin suppresses TNF-α-induced NF-κB activation and target gene expression

IL-1 promotes α-epithelial Sodium Channel (α-ENaC) expression in murine lung epithelial cells: involvement of NF-κB.

Protein Kinase Cζ Mediates Cigarette Smoke/Aldehyde- and Lipopolysaccharide-induced Lung Inflammation and Histone Modifications

Diesel Exhaust Particles Induce the Over expression of Tumor Necrosis Factor-α (TNF-α) Gene in Alveolar Macrophages and Failed to Induce Apoptosis through Activation of Nuclear Factor-κB (NF-κB)

Astragalus membranaceus Extract Attenuates Inflammation and Oxidative Stress in Intestinal Epithelial Cells via NF-κB Activation and Nrf2 Response

TNF Receptor-Associated Factor-2 Is Involved in Both IL-1β and TNF-α Signaling Cascades Leading to NF-κB Activation and IL-8 Expression in Human Intestinal Epithelial Cells

Multiwalled carbon nanotubes activate NF-κB and AP-1 signaling pathways to induce apoptosis in rat lung epithelial cells

Luteolin suppresses inflammation-associated gene expression by blocking NF-kappaB and AP-1 activation pathway in mouse alveolar macrophages.

HPV16 E2-mediated potentiation of NF-κB activation induced by TNF-α involves parallel activation of STAT3 with a reduction in E2-induced apoptosis

Oxidative stress and TNF-α induce histone acetylation and NF-κB/AP-1 activation in alveolar epithelial cells: Potential mechanism in gene transcription in lung inflammation