Hypoxia Antagonizes Glucose Deprivation on Interleukin 6 Expression in an Akt Dependent, but HIF-1/2α Independent Manner

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

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

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.

Original languageEnglish
Article numbere58662
JournalPLoS ONE
Volume8
Issue number3
DOIs
StatePublished - 8 Mar 2013

Fingerprint

Dive into the research topics of 'Hypoxia Antagonizes Glucose Deprivation on Interleukin 6 Expression in an Akt Dependent, but HIF-1/2α Independent Manner'. Together they form a unique fingerprint.

Cite this