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
Correspondence to : *Correspondence: jinpark@hallym.ac.kr
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 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.
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
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
Hojin Ryu, Carole Laffont, Florian Frugier, and Ildoo Hwang
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