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Mol. Cells 2012; 33(4): 335-341

Published online March 23, 2012

https://doi.org/10.1007/s10059-012-2287-0

© The Korean Society for Molecular and Cellular Biology

Extracellular HIV-1 Tat Induces Human Beta-Defensin-2 Production Via NF-kappaB/AP-1 Dependent Pathways in Human B Cells

Sung Mi Ju, Ah Ra Goh, Dong-Joo Kwon, Gi Soo Youn, Hyung-Joo Kwon1, Yong Soo Bae2,Soo Young Choi, and Jinseu Park*

Department of Biomedical Science, Research Institute for Bioscience and Biotechnology, Hallym University, Chunchon 200-702, Korea, 1Department of Microbiology, College of Medicine, Hallym University, Chunchon 200-702, Korea, 2Department of Biological Science, College of Natural Sciences, Sungkyunkwan University, Suwon 440-746, Korea

Correspondence to : *Correspondence: jinpark@hallym.ac.kr

Received: December 21, 2011; Revised: February 3, 2012; Accepted: February 6, 2012

Abstract

Defensins, a family of antimicrobial peptides, are one of the first lines of host defense. Human beta-defensins (hBD) such as hBD-2 and -3 have anti-HIV activity. Previ-ous studies have shown that HIV-1 virion can induce the expression of hBD, although the exact components of HIV-1 virion that are responsible for hBD expression have not yet been elucidated. In this study, we examined the effect of HIV-1 Tat on the expression of hBD in B cells. Stimulation of B cells with HIV-1 Tat protein significantly increased the mRNA and protein levels of hBD-2. HIV-1 Tat also induced the activation of a reporter gene for hBD-2 in a dose-dependent manner in B cells. Pretreatment of B cells with a JNK inhibitor suppressed HIV-1 Tat-induced hBD-2 expression. Pretreatment of B cells with AP-1 inhibitors or NF-?B inhibitors led to a decrease in HIV-1 Tat-induced protein and mRNA expression of hBD-2. Taken together, our results indicate that HIV-1 Tat can up-regulate the expression of hBD-2 via JNK-NF-?B/AP-1-dependent pathways in human B cells.

Keywords AP-1, B cells, beta-defensins, HIV, MAPK, NF-?B, Tat

Article

Research Article

Mol. Cells 2012; 33(4): 335-341

Published online April 30, 2012 https://doi.org/10.1007/s10059-012-2287-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Extracellular HIV-1 Tat Induces Human Beta-Defensin-2 Production Via NF-kappaB/AP-1 Dependent Pathways in Human B Cells

Sung Mi Ju, Ah Ra Goh, Dong-Joo Kwon, Gi Soo Youn, Hyung-Joo Kwon1, Yong Soo Bae2,Soo Young Choi, and Jinseu Park*

Department of Biomedical Science, Research Institute for Bioscience and Biotechnology, Hallym University, Chunchon 200-702, Korea, 1Department of Microbiology, College of Medicine, Hallym University, Chunchon 200-702, Korea, 2Department of Biological Science, College of Natural Sciences, Sungkyunkwan University, Suwon 440-746, Korea

Correspondence to:*Correspondence: jinpark@hallym.ac.kr

Received: December 21, 2011; Revised: February 3, 2012; Accepted: February 6, 2012

Abstract

Defensins, a family of antimicrobial peptides, are one of the first lines of host defense. Human beta-defensins (hBD) such as hBD-2 and -3 have anti-HIV activity. Previ-ous studies have shown that HIV-1 virion can induce the expression of hBD, although the exact components of HIV-1 virion that are responsible for hBD expression have not yet been elucidated. In this study, we examined the effect of HIV-1 Tat on the expression of hBD in B cells. Stimulation of B cells with HIV-1 Tat protein significantly increased the mRNA and protein levels of hBD-2. HIV-1 Tat also induced the activation of a reporter gene for hBD-2 in a dose-dependent manner in B cells. Pretreatment of B cells with a JNK inhibitor suppressed HIV-1 Tat-induced hBD-2 expression. Pretreatment of B cells with AP-1 inhibitors or NF-?B inhibitors led to a decrease in HIV-1 Tat-induced protein and mRNA expression of hBD-2. Taken together, our results indicate that HIV-1 Tat can up-regulate the expression of hBD-2 via JNK-NF-?B/AP-1-dependent pathways in human B cells.

Keywords: AP-1, B cells, beta-defensins, HIV, MAPK, NF-?B, Tat

Mol. Cells
Jun 30, 2023 Vol.46 No.6, pp. 329~398
COVER PICTURE
The cellular proteostasis network is adaptively modulated upon cellular stress, thereby protecting cells from proteostasis collapse. Heat shock induces the translocation of misfolded proteins and the chaperone protein HSP70 into nucleolus, where nuclear protein quality control primarily occurs. Nuclear RNA export factor 1 (green), nucleolar protein fibrillarin (red), and nuclei (blue) were visualized in NIH3T3 cells under basal (left) and heat shock (right) conditions (Park et al., pp. 374-386).

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