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

Published online April 30, 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
May 31, 2022 Vol.45 No.5, pp. 273~352
COVER PICTURE
Fe2+ ion depletion-induced expression of BΔGFP at the early stage of leaf development (Choi et al., pp. 294-305).

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