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Study of human neuronal mu‐opioid receptor gene expression under hypoxic condition
Author(s) -
Cook Ryan J,
Karch Christopher P,
Arslan Albert M,
Ko Jane L
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a284-a
Subject(s) - chromatin immunoprecipitation , hypoxia (environmental) , receptor , programmed cell death , apoptosis , biology , cell , microbiology and biotechnology , chromatin , transcription factor , gene expression , gene , chemistry , promoter , biochemistry , oxygen , organic chemistry
Hypoxia is a condition of insufficient oxygen supply. Among various cell types, neuronal cells are particularly vulnerable to hypoxia due to their high metabolic rates. In order to investigate the hypoxic effect on human neuronal system in detail, human neuronal (NMB) cells were treated with hypoxic mimic, desferoxamine (DFO). Cell viability tests demonstrated that 24 hr DFO treatment resulted in approximately 40 % of cell death and 50% inhibition of cell proliferation as compared to those of non‐treated groups (control). An up‐regulation of HIF‐1α messages in neuronal cells was evidence for the hypoxic condition via RT‐PCR̃ Recently opioids have been implicated to play roles in neuronal cell death and survival. The hypoxic effect on the neuronal mu‐opioid receptors (MOR) was therefore examined. RT‐PCR results demonstrated a down regulation of MOR message under hypoxic condition. The preliminary results of chromatin immunoprecipitation (ChIP) further indicated that the binding of Sp1 to MOR proximal promoter region was decreased during hypoxia, whereas an increase of Sp3 binding to the promoter was observed. These results implicated hypoxia altered/shifted the dynamic binding of transcription factors to the promoter region, resulting in a decrease of neuronal MOR gene expression.