Article
Suppressive effect on MDC and IP-10 expression in monocytes by endocrine disruptor chemicals.
Department of Family Medicine, Zuoying Armed Force General Hospital, Kaohsiung, Taiwan, Republic of China.
Inflammation (impact factor:
1.75).
09/2009;
33(1):10-7.
DOI:10.1007/s10753-009-9153-z
pp.10-7
Source: PubMed
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Citations (0)
- Cited In (2)
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Article: Chemokine (C-C motif) ligand 22 was down-regulated in a human B lymphoblastoid cell line by PCB153 and in residents from PCBs-contaminated areas.
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ABSTRACT: Polychlorinated biphenyls (PCBs) are ubiquitous, persistent pollutants found in the environment and human tissues. Exposure to PCBs is of great concern to human health because they are known to cause neurological, reproductive, endocrinal, and other effects. The aim of the present study was to find some novel gene markers induced by PCBs through a combination of microarray screening followed by validating with quantitative real time PCR in vitro and in population investigation. In the present study, gene expression profiles of human B lymphoblastoid cells treated with different concentrations of non-coplanar 2, 2', 4, 4', 5, 5'-hexachlorobiphenyl (PCB153) were analyzed using microarray. The differentially expressed genes were further confirmed by real-time PCR in vitro and in individuals from PCBs-contaminated sites. Our results indicated an overlap of 15 differentially expressed genes among samples treated with different concentrations of PCB153, and six of them were selected for validating with qRT-PCR. Two up-regulated genes (CCDC92 and TMEM175) and three down-regulated genes (CCL22, GZMK, and STK38L) were further confirmed by qRT-PCR in vitro. The expression levels of CCL22 in individuals from PCBs-contaminated sites were significantly (P<0.05) lower than those in controls. Therefore, CCL22 seems to be a sensitive gene marker induced by PCBs, although it needs to be confirmed by further studies with a larger number of subjects.Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 01/2013; · 2.85 Impact Factor -
Article: Prostaglandin I(2) analogues enhance growth-related oncogene-alpha expression in human monocyte-derived dendritic cells.
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ABSTRACT: Chemokines for neutrophils such as growth-related oncogene-alpha (GRO-alpha) are important in patients with refractory or severe asthma. Prostaglandin I(2) (PGI(2)) analogues were regarded as potential treatments for asthma. Dendritic cells (DCs) are the professional antigen-presenting cells and play a critical role in regulating immune response. However, it is unknown whether PGI(2) analogues have regulatory effects on GRO-alpha expression in human monocyte-derived DCs (MDDCs). The human MDDCs were pretreated with iloprost and treprostinil (two PGI(2) analogues) or forskolin, a cyclic adenosine monophosphate (cAMP) activator, before stimulation with lipopolysaccharide (LPS). In some cases, I prostanoid (IP) receptor and E prostanoid (EP) antagonists were pretreated before PGI(2) analogue treatment. To investigate the intracellular signaling, nuclear factor (NF)-kappaB inhibitor and the mitogen-activated protein kinase (MAPK) inhibitors were pretreated before PGI(2) analogue treatment. GRO-alpha was measured by enzyme-linked immunosorbent assay. Intracellular signaling was also investigated by Western blot. Iloprost and treprostinil enhanced LPS-induced GRO-alpha expression in MDDCs. This effect could be reversed by an I prostanoid receptor antagonist, CAY10449, but not EP receptor antagonists. Forskolin conferred a similar modulating effect as that noted in iloprost- and treprostinil-treated MDDCs. PGI(2) analogue-enhanced LPS-induced GRO-alpha expression was reduced by MAPK-p38 inhibitor, SB203580. PGI(2) analogues enhanced LPS-induced phospho-p38 expression. PGI(2) analogues enhanced LPS-induced GRO-alpha expression via the IP receptor-cAMP and p38-MAPK pathways in human MDDCs, which may further recruit neutrophil accumulation and adversely affect patients with refractory or severe asthma because of airway neutrophilia. These effects should be considered for PGI(2) analogues as candidates for the treatment of asthma.Inflammation 03/2010; 33(5):334-43. · 1.75 Impact Factor
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Keywords
4-octylphenol suppressed LPS-induced MDC expression
chemokine expression
CXCL10/ IFN-alpha-inducible protein 10
EDC-mediated signaling events
endocrine disrupter chemicals
histone H4 acetylation
inflammatory response
IP-10 expression
leukocyte recruitment
LPS-induced acetylated histone 4
LPS-induced activation
LPS-induced MDC
MAPK signaling pathway
MDC gene loci
MKK1/2-ERK MAPK pathway
monocyte-derived chemokine
potential impact
Th1 chemokine
Th2 chemokine
Th2-related chemokines