The Experts below are selected from a list of 24 Experts worldwide ranked by ideXlab platform
Taeg Kyu Kwon - One of the best experts on this subject based on the ideXlab platform.
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high mobility group box 1 protein induces Mucin 8 expression through the activation of the jnk and pi3k akt signal pathways in human airway epithelial cells
Biochemical and Biophysical Research Communications, 2012Co-Authors: Taeg Kyu KwonAbstract:High-mobility group box-1 protein (HMGB1), which is produced by immune cells, was recently identified as a proinflammatory mediator in various inflammatory diseases. In this study, we investigated the effect of HMGB1 on the expression of Mucin (MUC) genes in human airway epithelial cells. We showed that HMGB1 markedly increased MUC8 expression, and that the expression of other MUC genes was also regulated by HMGB1. HMGB1 activated the JNK and PI3K/Akt signaling pathways, and inhibitors of JNK and PI3K/Akt markedly inhibited HMGB1-induced MUC8 expression. Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS). However, the ROS scavengers Trolox and N-acetylcysteine (NAC) had no effect on MUC8 expression in HMGB1-treated NCI-H292 cells. Taken together, our results suggest that HMGB1 induces MUC8 expression in a JNK and PI3K/Akt signaling pathway-dependent manner but that HMGB1 acts in an ROS-independent manner.
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High-mobility group box-1 protein induces Mucin 8 expression through the activation of the JNK and PI3K/Akt signal pathways in human airway epithelial cells.
Biochemical and biophysical research communications, 2012Co-Authors: Dong-eun Kim, Kyoung-jin Min, Jung Soo Kim, Taeg Kyu KwonAbstract:High-mobility group box-1 protein (HMGB1), which is produced by immune cells, was recently identified as a proinflammatory mediator in various inflammatory diseases. In this study, we investigated the effect of HMGB1 on the expression of Mucin (MUC) genes in human airway epithelial cells. We showed that HMGB1 markedly increased MUC8 expression, and that the expression of other MUC genes was also regulated by HMGB1. HMGB1 activated the JNK and PI3K/Akt signaling pathways, and inhibitors of JNK and PI3K/Akt markedly inhibited HMGB1-induced MUC8 expression. Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS). However, the ROS scavengers Trolox and N-acetylcysteine (NAC) had no effect on MUC8 expression in HMGB1-treated NCI-H292 cells. Taken together, our results suggest that HMGB1 induces MUC8 expression in a JNK and PI3K/Akt signaling pathway-dependent manner but that HMGB1 acts in an ROS-independent manner.
Dong-eun Kim - One of the best experts on this subject based on the ideXlab platform.
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High-mobility group box-1 protein induces Mucin 8 expression through the activation of the JNK and PI3K/Akt signal pathways in human airway epithelial cells.
Biochemical and biophysical research communications, 2012Co-Authors: Dong-eun Kim, Kyoung-jin Min, Jung Soo Kim, Taeg Kyu KwonAbstract:High-mobility group box-1 protein (HMGB1), which is produced by immune cells, was recently identified as a proinflammatory mediator in various inflammatory diseases. In this study, we investigated the effect of HMGB1 on the expression of Mucin (MUC) genes in human airway epithelial cells. We showed that HMGB1 markedly increased MUC8 expression, and that the expression of other MUC genes was also regulated by HMGB1. HMGB1 activated the JNK and PI3K/Akt signaling pathways, and inhibitors of JNK and PI3K/Akt markedly inhibited HMGB1-induced MUC8 expression. Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS). However, the ROS scavengers Trolox and N-acetylcysteine (NAC) had no effect on MUC8 expression in HMGB1-treated NCI-H292 cells. Taken together, our results suggest that HMGB1 induces MUC8 expression in a JNK and PI3K/Akt signaling pathway-dependent manner but that HMGB1 acts in an ROS-independent manner.
Yoonseok Choi - One of the best experts on this subject based on the ideXlab platform.
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cadmium induces Mucin 8 expression via toll like receptor 4 mediated extracellular signal related kinase 1 2 and p38 mitogen activated protein kinase in human airway epithelial cells
International Forum of Allergy & Rhinology, 2016Co-Authors: Siyoun Song, Yoonseok ChoiAbstract:Background Inhalation of cadmium can lead to development of inflammatory airway diseases such as acute pulmonary edema and chronic obstructive pulmonary disease. In inflammatory airway diseases, expression of Mucins is increased, which leads to increased morbidity and mortality of the affected patients. However, no study on the effect of cadmium on expression of Mucin genes in airway epithelial cells has been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of cadmium on expression of Mucin genes in human airway epithelial cells. Methods In Mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effect and signaling pathway of cadmium on expression of Mucin genes were investigated using reverse transcription–polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA). Results Cadmium increased Mucin 8 (MUC8) expression and Toll-like receptor (TLR) 4 messenger RNA (mRNA) expression. Cadmium significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, TLR4 siRNA, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked cadmium-induced MUC8 mRNA expression. TLR4 siRNA significantly blocked cadmium-activated phosphorylation of ERK1/2 MAPK and p38 MAPK. Conclusion The results of this study suggest for the first time that cadmium induces MUC8 expression via TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells.
Kyoung-jin Min - One of the best experts on this subject based on the ideXlab platform.
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High-mobility group box-1 protein induces Mucin 8 expression through the activation of the JNK and PI3K/Akt signal pathways in human airway epithelial cells.
Biochemical and biophysical research communications, 2012Co-Authors: Dong-eun Kim, Kyoung-jin Min, Jung Soo Kim, Taeg Kyu KwonAbstract:High-mobility group box-1 protein (HMGB1), which is produced by immune cells, was recently identified as a proinflammatory mediator in various inflammatory diseases. In this study, we investigated the effect of HMGB1 on the expression of Mucin (MUC) genes in human airway epithelial cells. We showed that HMGB1 markedly increased MUC8 expression, and that the expression of other MUC genes was also regulated by HMGB1. HMGB1 activated the JNK and PI3K/Akt signaling pathways, and inhibitors of JNK and PI3K/Akt markedly inhibited HMGB1-induced MUC8 expression. Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS). However, the ROS scavengers Trolox and N-acetylcysteine (NAC) had no effect on MUC8 expression in HMGB1-treated NCI-H292 cells. Taken together, our results suggest that HMGB1 induces MUC8 expression in a JNK and PI3K/Akt signaling pathway-dependent manner but that HMGB1 acts in an ROS-independent manner.
Jung Soo Kim - One of the best experts on this subject based on the ideXlab platform.
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High-mobility group box-1 protein induces Mucin 8 expression through the activation of the JNK and PI3K/Akt signal pathways in human airway epithelial cells.
Biochemical and biophysical research communications, 2012Co-Authors: Dong-eun Kim, Kyoung-jin Min, Jung Soo Kim, Taeg Kyu KwonAbstract:High-mobility group box-1 protein (HMGB1), which is produced by immune cells, was recently identified as a proinflammatory mediator in various inflammatory diseases. In this study, we investigated the effect of HMGB1 on the expression of Mucin (MUC) genes in human airway epithelial cells. We showed that HMGB1 markedly increased MUC8 expression, and that the expression of other MUC genes was also regulated by HMGB1. HMGB1 activated the JNK and PI3K/Akt signaling pathways, and inhibitors of JNK and PI3K/Akt markedly inhibited HMGB1-induced MUC8 expression. Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS). However, the ROS scavengers Trolox and N-acetylcysteine (NAC) had no effect on MUC8 expression in HMGB1-treated NCI-H292 cells. Taken together, our results suggest that HMGB1 induces MUC8 expression in a JNK and PI3K/Akt signaling pathway-dependent manner but that HMGB1 acts in an ROS-independent manner.