Logo image
Macrophage Colony Stimulating Factor Regulation by Nuclear Factor Kappa B: A Relevant Pathway in Human Immunodeficiency Virus Type 1 Infected Macrophages
Journal article   Open access   Peer reviewed

Macrophage Colony Stimulating Factor Regulation by Nuclear Factor Kappa B: A Relevant Pathway in Human Immunodeficiency Virus Type 1 Infected Macrophages

Michael Kogan, Valerie Haine, Yuxong Ke, Brian Wigdahl, Tracy Fischer-Smith and Jay Rappaport
DNA and cell biology, v 31(3), pp 28-289
01 Mar 2012
PMID: 21895511
url
https://doi.org/10.1089/dna.2011.1357View
Published, Version of Record (VoR) Open

Abstract

Molecular Mechanisms of Disease
Macrophage colony stimulating factor (M-CSF) is a cytokine that promotes monocyte differentiation and survival. When overexpressed, M-CSF contributes to pathology in a wide variety of diseases, including osteoporosis, obesity, certain human cancers, and in human immunodeficiency virus type 1 (HIV-1) infection, particularly with respect to monocyte/macrophage infection and the development of HIV-1 associated central nervous system disorders. In this study, our aim was to expand the current knowledge of M-CSF regulation, focusing on nuclear factor kappa B (NF-κB), a transcription factor playing a prominent role during inflammation and HIV-1 infection. Our results suggest that tumor necrosis factor alpha (TNF-α) promotes M-CSF secretion in primary macrophages and activates the −1310/+48 bp M-CSF promoter in Mono-Mac 1 cells. Inhibitors of the NF-κB pathway diminish this response. We identified four putative NF-κB and four CCAAT-enhancer-binding protein beta binding sites within the M-CSF promoter. Our findings, using promoter constructs mutated at individual NF-κB sites within the M-CSF promoter region, suggest that these sites are redundant with respect to NF-κB regulation. TNF-α treatment promoted NF-κB p65 binding to the M-CSF promoter in phorbol 12-myristate 13-acetate (PMA) treated U937 cells chronically infected with HIV-1 (U1 cells), but not in PMA treated uninfected U937 cells, suggesting that the presence of HIV-1 increases the NF-κB response. In conclusion, our findings demonstrate that NF-κB induces M-CSF expression on a promoter level via multiple functional NF-κB binding sites and that this pathway is likely relevant in HIV-1 infection of macrophages.

Metrics

9 Record Views
17 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Cell Biology
Genetics & Heredity
Logo image