Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner.
Although both glucose deprivation and hypoxia have been reported to promote cascades of biological alterations that lead to induction of inflammatory mediators, we hypothesized that glucose deprivation and hypoxia might show neutral, synergistic or antagonistic effects to each other on gene expressi...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3592797?pdf=render |
| _version_ | 1819022297577553920 |
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| author | Sung Ji Choi Ik Jae Shin Kang-Hoon Je Eun Kyoung Min Eun Ji Kim Hee-Sun Kim Senyon Choe Dong-Eog Kim Dong Kun Lee |
| author_facet | Sung Ji Choi Ik Jae Shin Kang-Hoon Je Eun Kyoung Min Eun Ji Kim Hee-Sun Kim Senyon Choe Dong-Eog Kim Dong Kun Lee |
| author_sort | Sung Ji Choi |
| collection | DOAJ |
| description | Although both glucose deprivation and hypoxia have been reported to promote cascades of biological alterations that lead to induction of inflammatory mediators, we hypothesized that glucose deprivation and hypoxia might show neutral, synergistic or antagonistic effects to each other on gene expression of inflammatory mediators depending on the regulatory components in their promoters. Gene expression of interleukin 6 (IL-6) was analyzed by real-time PCR, ELISA, or Western blot. Effects of glucose deprivation and/or hypoxia on activation of signaling pathways were analyzed by time-dependent phosphorylation patterns of signaling molecules. We demonstrate that hypoxia antagonized the effects of glucose deprivation on induction of IL-6 gene expression in microglia, macrophages, and monocytes. Hypoxia also antagonized thapsigargin-induced IL-6 gene expression. Hypoxia enhanced phosphorylation of Akt, and inhibition of Akt was able to reverse the effects of hypoxia on IL-6 gene expression. However, inhibition of HIF-1/2α did not reverse the effects of hypoxia on IL-6 gene expression. In addition, phosphorylation of p38, but not JNK, was responsible for the effects of glucose deprivation on IL-6 gene expression. |
| first_indexed | 2024-12-21T04:20:46Z |
| format | Article |
| id | doaj.art-1bb73715bad844848b176e9733173a84 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-21T04:20:46Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-1bb73715bad844848b176e9733173a842022-12-21T19:16:10ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0183e5866210.1371/journal.pone.0058662Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner.Sung Ji ChoiIk Jae ShinKang-Hoon JeEun Kyoung MinEun Ji KimHee-Sun KimSenyon ChoeDong-Eog KimDong Kun LeeAlthough both glucose deprivation and hypoxia have been reported to promote cascades of biological alterations that lead to induction of inflammatory mediators, we hypothesized that glucose deprivation and hypoxia might show neutral, synergistic or antagonistic effects to each other on gene expression of inflammatory mediators depending on the regulatory components in their promoters. Gene expression of interleukin 6 (IL-6) was analyzed by real-time PCR, ELISA, or Western blot. Effects of glucose deprivation and/or hypoxia on activation of signaling pathways were analyzed by time-dependent phosphorylation patterns of signaling molecules. We demonstrate that hypoxia antagonized the effects of glucose deprivation on induction of IL-6 gene expression in microglia, macrophages, and monocytes. Hypoxia also antagonized thapsigargin-induced IL-6 gene expression. Hypoxia enhanced phosphorylation of Akt, and inhibition of Akt was able to reverse the effects of hypoxia on IL-6 gene expression. However, inhibition of HIF-1/2α did not reverse the effects of hypoxia on IL-6 gene expression. In addition, phosphorylation of p38, but not JNK, was responsible for the effects of glucose deprivation on IL-6 gene expression.http://europepmc.org/articles/PMC3592797?pdf=render |
| spellingShingle | Sung Ji Choi Ik Jae Shin Kang-Hoon Je Eun Kyoung Min Eun Ji Kim Hee-Sun Kim Senyon Choe Dong-Eog Kim Dong Kun Lee Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner. PLoS ONE |
| title | Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner. |
| title_full | Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner. |
| title_fullStr | Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner. |
| title_full_unstemmed | Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner. |
| title_short | Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner. |
| title_sort | hypoxia antagonizes glucose deprivation on interleukin 6 expression in an akt dependent but hif 1 2α independent manner |
| url | http://europepmc.org/articles/PMC3592797?pdf=render |
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