Extracellular HIV-1 Tat up-regulates expression of matrix metalloproteinase-9 via a MAPK-NF-κB dependent pathway in human astrocytes

Ju, Sung Mi; Song, Ha Yong; Lee, Ji Ae; Lee, Su Jin; Choi, Soo Young; Park, Jinseu

doi:10.3858/emm.2009.41.2.011

Cited by 72 publications

(61 citation statements)

References 31 publications

(33 reference statements)

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“…Previous studies have shown that HIV-1 infection can activate the host cellular MAPK signaling pathway, and again, conversely, an activated MAPK signal pathway can enhance HIV-1 infection efficiency [11,12,18,26] .…”

Section: Discussionmentioning

confidence: 97%

Down-regulation of HIV-1 infection by inhibition of the MAPK signaling pathway

et al. 2011

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The human immunodeficiency virus type 1 (HIV-1) can interact with and exploit the host cellular machinery to replicate and propagate itself. Numerous studies have shown that the Mitogen-activated protein kinase (MAPK) signal pathway can positively regulate the replication of HIV-1, but exactly how each MAPK pathway affects HIV-1 infection and replication is not understood. In this study, we used the Extracellular signal-regulated kinase (ERK) pathway inhibitor, PD98059, the Jun N-terminal kinase (JNK) pathway inhibitor, SP600125, and the p38 pathway inhibitor, SB203580, to investigate the roles of these pathways in HIV-1 replication. We found that application of PD98059 results in a strong VSV-G pseudotyped HIV-1(NL4-3) luciferase reporter virus and HIV-1(NL4-3) virus inhibition activity. In addition, SB203580 and SP600125 also elicited marked VSV-G pseudotyped HIV-1(NL4-3) luciferase reporter virus inhibition activity but no HIV-1(NL4-3) virus inhibition activity. We also found that SB203580 and SP600125 can enhance the HIV-1 inhibition activity of PD98059 when cells were treated with all three MAPK pathway inhibitors in combination. Finally, we show that HIV-1 virus inhibition activity of the MAPK pathway inhibitors was the result of the negative regulation of HIV-1 LTR promoter activity.

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Section: Discussionmentioning

confidence: 97%

Down-regulation of HIV-1 infection by inhibition of the MAPK signaling pathway

et al. 2011

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“…Assay of MMP-9 activity by gelatin zymography MMP-9 activity was assessed by gelatin zymography as described previously (25). Briefly, cells were pretreated with control SOD (2 μM) or Tat-SOD (0.5, 1, and 2 μM) for 1 h, followed by exposure to TNF-α (10 ng/ml) for the indicated periods.…”

Section: Rt-pcr Analysismentioning

confidence: 99%

Suppression of TNF-alpha-induced MMP-9 expression by a cell-permeable superoxide dismutase in keratinocytes

Song

Ju²,

Goh³

et al. 2011

BMB Reports

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“…Tat is a regulatory protein which enhances viral transcription, RNA processing, and efficient viral replication (140, 219), with additional immune-modulatory effects on cytokine expression (e.g., IL-10, IL-6, TNF-α) and promotion of T cell apoptosis (3, 15, 39, 120, 274). Like Vpr, Tat is secreted by infected cells, can enter uninfected cells, and may exert local paracrine effects as well as circulating at detectable levels in the serum (36, 66, 270).…”

Section: Hiv Infection Adipogenesis and Adipocyte Functionmentioning

confidence: 99%

Adipose Tissue in HIV Infection

Koethe

2017

Comprehensive Physiology

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HIV infection and antiretroviral therapy (ART) treatment exert diverse effects on adipocytes and stromal-vascular fraction cells, leading to changes in adipose tissue quantity, distribution, and energy storage. A HIV-associated lipodystrophic condition was recognized early in the epidemic, characterized by clinically apparent changes in subcutaneous, visceral, and dorsocervical adipose depots. Underlying these changes is altered adipose tissue morphology and expression of genes central to adipocyte maturation, regulation, metabolism, and cytokine signaling. HIV viral proteins persist in circulation and locally within adipose tissue despite suppression of plasma viremia on ART, and exposure to these proteins impairs preadipocyte maturation and reduces adipocyte expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) and other genes involved in cell regulation. Several early nucleoside reverse transcriptase inhibitor and protease inhibitor antiretroviral drugs demonstrated substantial adipocyte toxicity, including reduced mitochondrial DNA content and respiratory chain enzymes, reduced PPAR-γ and other regulatory gene expression, and increased pro-inflammatory cytokine production. Newer-generation agents, such as integrase inhibitors, appear to have fewer adverse effects. HIV infection also alters the balance of CD4+ and CD8+ T cells in adipose tissue, with effects on macrophage activation and local inflammation, while the presence of latently-infected CD4+ T cells in adipose tissue may constitute a protected viral reservoir. This review provides a synthesis of the literature on how HIV virus, ART treatment, and host characteristics interact to affect adipose tissue distribution, immunology, and contribution to metabolic health, and adipocyte maturation, cellular regulation, and energy storage.

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Extracellular HIV-1 Tat up-regulates expression of matrix metalloproteinase-9 via a MAPK-NF-κB dependent pathway in human astrocytes

Cited by 72 publications

References 31 publications

Down-regulation of HIV-1 infection by inhibition of the MAPK signaling pathway

Down-regulation of HIV-1 infection by inhibition of the MAPK signaling pathway

Suppression of TNF-alpha-induced MMP-9 expression by a cell-permeable superoxide dismutase in keratinocytes

Adipose Tissue in HIV Infection

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