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Histone deacetylase inhibitors up-regulate LL-37 expression independent of toll-like receptor mediated signalling in airway epithelial cells.

Liu Q, Liu J, Roschmann KI, van Egmond D, Golebski K, Fokkens WJ, Wang D, van Drunen CM - J Inflamm (Lond) (2013)

Bottom Line: Our results showed that HDAC inhibitors up-regulated LL-37 gene expression independent of poly (I:C) stimulation in PNEC as well as in NCI-H292 cells.HDAC inhibitors increased LL37 protein expression in NCI-H292 cells but not in PNEC.In conclusion, HDAC inhibitors directly up-regulated LL-37 gene expression in human airway epithelial cells.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Otolaryngology, Eye, Ear, Nose and Throat Hospital, Fudan University, Shanghai, 200031, China. wangdehuient@sina.com.

ABSTRACT
HDAC inhibitors have been proposed as anticancer agents. However, their roles in innate genes expression remain not well known. Cathelicidin LL-37 is one of the few human bactericidal peptides, but the regulation of histone acetylation on LL-37 expression in airway epithelium remains largely unknown. Therefore, we investigated the effects of two non-selective HDACi, trichostatin A (TSA) and sodium butyrate (SB), on the expression of the cathelicidin LL-37 in human airway epithelial cells. LL37 in human NCI-H292 airway epithelial cells and the primary cultures of normal nasal epithelial cells(PNEC) in response to HDAC inhibitors with or without poly (I:C) stimulation was assessed using real-time PCR and western blot. In parallel, IL-6 expression was evaluated by ELISA. Our results showed that HDAC inhibitors up-regulated LL-37 gene expression independent of poly (I:C) stimulation in PNEC as well as in NCI-H292 cells. HDAC inhibitors increased LL37 protein expression in NCI-H292 cells but not in PNEC. In addition, HDAC inhibitors significantly inhibited poly (I:C)-induced IL-6 production in both of the epithelial cells. In conclusion, HDAC inhibitors directly up-regulated LL-37 gene expression in human airway epithelial cells.

No MeSH data available.


The LL37 protein expression induced by HDAC inhibitors in the NCI-H292 cells and the primary nasal epithelial cells. Whole cell lysates prepared from the NCI-H292 cells and PNEC 24 h after treatment with TSA(200 nM) and SB(4 mM). Data shown are from a single representative experiment. These experiments were repeated at least twice to confirm reproducibility.
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Figure 3: The LL37 protein expression induced by HDAC inhibitors in the NCI-H292 cells and the primary nasal epithelial cells. Whole cell lysates prepared from the NCI-H292 cells and PNEC 24 h after treatment with TSA(200 nM) and SB(4 mM). Data shown are from a single representative experiment. These experiments were repeated at least twice to confirm reproducibility.

Mentions: To analyse the effect of HDAC inhibitors on the LL37 protein expression in the epithelial cells, we treated the NCI-H292 cells and human primary nasal epithelial cells with HDAC inhibitors for 24 hours, followed by the extract of cell total protein and western blot analysis. Our results indicated that the two HDAC inhibitors induced LL37 protein expression in the NCI-H292 cells. However, no significant difference of LL37 protein expression was found in the primary cells (Figure 3).


Histone deacetylase inhibitors up-regulate LL-37 expression independent of toll-like receptor mediated signalling in airway epithelial cells.

Liu Q, Liu J, Roschmann KI, van Egmond D, Golebski K, Fokkens WJ, Wang D, van Drunen CM - J Inflamm (Lond) (2013)

The LL37 protein expression induced by HDAC inhibitors in the NCI-H292 cells and the primary nasal epithelial cells. Whole cell lysates prepared from the NCI-H292 cells and PNEC 24 h after treatment with TSA(200 nM) and SB(4 mM). Data shown are from a single representative experiment. These experiments were repeated at least twice to confirm reproducibility.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3643837&req=5

Figure 3: The LL37 protein expression induced by HDAC inhibitors in the NCI-H292 cells and the primary nasal epithelial cells. Whole cell lysates prepared from the NCI-H292 cells and PNEC 24 h after treatment with TSA(200 nM) and SB(4 mM). Data shown are from a single representative experiment. These experiments were repeated at least twice to confirm reproducibility.
Mentions: To analyse the effect of HDAC inhibitors on the LL37 protein expression in the epithelial cells, we treated the NCI-H292 cells and human primary nasal epithelial cells with HDAC inhibitors for 24 hours, followed by the extract of cell total protein and western blot analysis. Our results indicated that the two HDAC inhibitors induced LL37 protein expression in the NCI-H292 cells. However, no significant difference of LL37 protein expression was found in the primary cells (Figure 3).

Bottom Line: Our results showed that HDAC inhibitors up-regulated LL-37 gene expression independent of poly (I:C) stimulation in PNEC as well as in NCI-H292 cells.HDAC inhibitors increased LL37 protein expression in NCI-H292 cells but not in PNEC.In conclusion, HDAC inhibitors directly up-regulated LL-37 gene expression in human airway epithelial cells.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Otolaryngology, Eye, Ear, Nose and Throat Hospital, Fudan University, Shanghai, 200031, China. wangdehuient@sina.com.

ABSTRACT
HDAC inhibitors have been proposed as anticancer agents. However, their roles in innate genes expression remain not well known. Cathelicidin LL-37 is one of the few human bactericidal peptides, but the regulation of histone acetylation on LL-37 expression in airway epithelium remains largely unknown. Therefore, we investigated the effects of two non-selective HDACi, trichostatin A (TSA) and sodium butyrate (SB), on the expression of the cathelicidin LL-37 in human airway epithelial cells. LL37 in human NCI-H292 airway epithelial cells and the primary cultures of normal nasal epithelial cells(PNEC) in response to HDAC inhibitors with or without poly (I:C) stimulation was assessed using real-time PCR and western blot. In parallel, IL-6 expression was evaluated by ELISA. Our results showed that HDAC inhibitors up-regulated LL-37 gene expression independent of poly (I:C) stimulation in PNEC as well as in NCI-H292 cells. HDAC inhibitors increased LL37 protein expression in NCI-H292 cells but not in PNEC. In addition, HDAC inhibitors significantly inhibited poly (I:C)-induced IL-6 production in both of the epithelial cells. In conclusion, HDAC inhibitors directly up-regulated LL-37 gene expression in human airway epithelial cells.

No MeSH data available.