Up-regulation of human β-defensin 2 by interleukin-1β in A549 cells: involvement of PI3K, PKC, p38 MAPK, JNK, and NF-κB

Jang, Byeong‐Churl; Lim, Ki-Jo; Paik, Jihye; Kwon, Young-Kyu; Shin, Sang-Woo; Kim, Sang-Chan; Jung, Tae‐Young; Kwon, Taeg Kyu; Cho, Jae-We; Baek, Won-Ki; Kim, Sang-Pyo; Suh, Min-Ho; Suh, Seong-Il

doi:10.1016/j.bbrc.2004.06.049

Cited by 59 publications

(85 citation statements)

References 36 publications

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“…Human β-defensins (hBD) found in the skin were the focus of this study (10)(11)(12). Currently, four hBD of different characteristics have been identified (13)(14)(15)(16)(17)(18)(19). These defensins have demonstrated the capability to kill and/or inactivate a spectrum of bacteria, fungi and enveloped viruses in vitro (12).…”

Section: Introductionmentioning

confidence: 99%

High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-3 Expression in Keratinocytes

Lan

Huang

et al. 2011

Mol Med

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Diabetes mellitus is characterized by elevated plasma glucose and increased rates of skin infections. Altered immune responses have been suggested to contribute to this prevalent complication, which involves microbial invasion. In this study we explored the effects of a high-glucose environment on the innate immunity of keratinocytes by focusing on β defensin-3 (BD3) using in vivo and in vitro models. Our results demonstrated that the perilesional skins of diabetic rats failed to show enhanced BD3 expression after wounding. In addition, high-glucose treatment reduced human BD3 (hBD3) expression of cultured human keratinocytes. This pathogenic process involved inhibition of p38MAPK signaling, an event that resulted from increased formation of advanced glycation end products. On the other hand, toll-like receptor-2 expression and function of cultured keratinocytes were not significantly affected by high-glucose treatment. In summary, high-glucose conditions inhibited the BD3 expression of epidermal keratinocytes, which in turn contributed to the frequent occurrences of infection associated with diabetic wounding.

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Section: Introductionmentioning

confidence: 99%

High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-3 Expression in Keratinocytes

Lan

Huang

et al. 2011

Mol Med

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“…Whole cell extracts were prepared in the lysis buffer as described previously [13]. Protein extracts were subject to SDS-PAGE (10% gel), transferred to nitrocellulose membranes (Schleicher & Schuell, NH), and probed with antibodies.…”

Section: Western Blotmentioning

confidence: 99%

Interferon regulatory factor‐1 is prerequisite to the constitutive expression and IFN‐γ‐induced upregulation of B7‐H1 (CD274)

et al. 2006

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Majority of cancer cells upregulate co-inhibitory molecule B7-H1 which confers resistance to anti-tumor immunity, allowing cancers to escape from host immune surveillance. We addressed the molecular mechanism underlying the regulation of cancer-associated B7-H1 expression in response to interferon-c (IFN-c). Using promoter constructs in luciferase assay, the region between 202 and 320 bp from the translational start site is responsible for B7-H1 expression. Electrophoretic mobility shift assay, site-directed mutagenesis and knockdown experiment using siRNA revealed that interferon regulatory factor-1 (IRF-1) is primarily responsible for the constitutive B7-H1 expression as well as for the IFN-c-mediated B7-H1 upregulation in a human lung cancer cell line A549. Additionally, AG490, a Janus activated kinase/signal transducer and activator of transcription inhibitor, greatly abolished the responsiveness of A549 cells to IFN-c by reducing the IRF-1 transcription. Our findings support a critical role of IRF-1 in the regulation of constitutive and IFN-c-induced expression of B7-H1 in cancer cells.

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“…The mitogen-activated protein kinases (MAPKs) such as p38, JNK and ERK protein kinase are involved in the signaling cascades leading to hBD-2 expression upon various stimuli (Jang et al, 2004;Méndez-Samperio et al, 2007;Yoon et al, 2010). We observed that JNK inhibitor, but not ERK and p38 MAPK inhibitors, suppressed HIV-1 Tat-induced mRNA expression of hBD-2 as well as the production of hBD-2 ( Fig.…”

Section: Discussionmentioning

confidence: 87%

“…Previous studies have indicated that the activity of MAP kinases such as p38, JNK and ERK protein kinase is involved in hBD-2 expression upon various stimuli (Jang et al, 2004;Méndez-Samperio et al, 2007;Yoon et al, 2010). To further analyze the effect of the MAPK superfamily pathway on HIV-1 Tat-mediated hBD-2 production, we measured HIV-1 Tat-induced hBD-2 production in the presence of pathway-specific inhibitors.…”

Section: Hiv-1 Tat Induced Jnk Activation That Is Required For Hbd-2 mentioning

confidence: 99%

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

Goh

Kwon

et al. 2012

Molecules and Cells

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Up-regulation of human β-defensin 2 by interleukin-1β in A549 cells: involvement of PI3K, PKC, p38 MAPK, JNK, and NF-κB

Cited by 59 publications

References 36 publications

High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-3 Expression in Keratinocytes

High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-3 Expression in Keratinocytes

Interferon regulatory factor‐1 is prerequisite to the constitutive expression and IFN‐γ‐induced upregulation of B7‐H1 (CD274)

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

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