Increased expression of opioid delta receptors by deoxy conformation heme proteins in NG108-15 cells

Kimberly P. Mayfield, Robert Horvath, Josephine Lai, Frank Porreca

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Adaptations to prolonged hypoxia include an increase in the expression of proteins that may facilitate survival. One mechanism by which hypoxia increases protein expression involves a change of heme proteins from oxygenated to deoxygenated conformations. In the present study, we tested the hypothesis that treatment of NG108-15 cells with metallic cations, which are known to induce a deoxygenated conformation of heme proteins, would increase delta opioid receptor (DOR) expression. Cells were treated with cobalt and nickel, which induce deoxygenated heme protein conformation, or zinc as a control for 48 h prior to quantifying DOR expression. Cobalt and nickel, but not zinc, significantly increased DOR expression. Heme synthesis inhibitors would block the synthesis of cobalt-substituted heme proteins which are locked in a deoxygenated conformation. The cobalt-induced increase in DOR expression was blocked by the heme synthesis inhibitor, 4,6-dioxoheptanoic acid. These experiments indicate that deoxygenated conformation heme proteins, which are thought to partially mimic hypoxia, increase DOR expression. The increase in DOR expression suggests that the DOR gene may be hypoxia-sensitive. Further, the increase in DOR expression suggests a potential adaptation strategy to hypoxia and may represent one of the first findings of physiological regulation of DOR expression.

Original languageEnglish (US)
Pages (from-to)358-362
Number of pages5
JournalBrain Research
Volume676
Issue number2
DOIs
StatePublished - Apr 10 1995

Fingerprint

Hemeproteins
delta Opioid Receptor
Cobalt
Nickel
Heme
Zinc
Protein Conformation
Cations
Proteins
Hypoxia

Keywords

  • 4,6-Dioxoheptanoic acid
  • Cobalt
  • Heme protein
  • Hypoxia
  • Naltrindole
  • NG108-15 cell
  • δ Opioid receptor

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Increased expression of opioid delta receptors by deoxy conformation heme proteins in NG108-15 cells. / Mayfield, Kimberly P.; Horvath, Robert; Lai, Josephine; Porreca, Frank.

In: Brain Research, Vol. 676, No. 2, 10.04.1995, p. 358-362.

Research output: Contribution to journalArticle

Mayfield, Kimberly P. ; Horvath, Robert ; Lai, Josephine ; Porreca, Frank. / Increased expression of opioid delta receptors by deoxy conformation heme proteins in NG108-15 cells. In: Brain Research. 1995 ; Vol. 676, No. 2. pp. 358-362.
@article{923e97fc98a04647a10324685476ba88,
title = "Increased expression of opioid delta receptors by deoxy conformation heme proteins in NG108-15 cells",
abstract = "Adaptations to prolonged hypoxia include an increase in the expression of proteins that may facilitate survival. One mechanism by which hypoxia increases protein expression involves a change of heme proteins from oxygenated to deoxygenated conformations. In the present study, we tested the hypothesis that treatment of NG108-15 cells with metallic cations, which are known to induce a deoxygenated conformation of heme proteins, would increase delta opioid receptor (DOR) expression. Cells were treated with cobalt and nickel, which induce deoxygenated heme protein conformation, or zinc as a control for 48 h prior to quantifying DOR expression. Cobalt and nickel, but not zinc, significantly increased DOR expression. Heme synthesis inhibitors would block the synthesis of cobalt-substituted heme proteins which are locked in a deoxygenated conformation. The cobalt-induced increase in DOR expression was blocked by the heme synthesis inhibitor, 4,6-dioxoheptanoic acid. These experiments indicate that deoxygenated conformation heme proteins, which are thought to partially mimic hypoxia, increase DOR expression. The increase in DOR expression suggests that the DOR gene may be hypoxia-sensitive. Further, the increase in DOR expression suggests a potential adaptation strategy to hypoxia and may represent one of the first findings of physiological regulation of DOR expression.",
keywords = "4,6-Dioxoheptanoic acid, Cobalt, Heme protein, Hypoxia, Naltrindole, NG108-15 cell, δ Opioid receptor",
author = "Mayfield, {Kimberly P.} and Robert Horvath and Josephine Lai and Frank Porreca",
year = "1995",
month = "4",
day = "10",
doi = "10.1016/0006-8993(95)00089-9",
language = "English (US)",
volume = "676",
pages = "358--362",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Increased expression of opioid delta receptors by deoxy conformation heme proteins in NG108-15 cells

AU - Mayfield, Kimberly P.

AU - Horvath, Robert

AU - Lai, Josephine

AU - Porreca, Frank

PY - 1995/4/10

Y1 - 1995/4/10

N2 - Adaptations to prolonged hypoxia include an increase in the expression of proteins that may facilitate survival. One mechanism by which hypoxia increases protein expression involves a change of heme proteins from oxygenated to deoxygenated conformations. In the present study, we tested the hypothesis that treatment of NG108-15 cells with metallic cations, which are known to induce a deoxygenated conformation of heme proteins, would increase delta opioid receptor (DOR) expression. Cells were treated with cobalt and nickel, which induce deoxygenated heme protein conformation, or zinc as a control for 48 h prior to quantifying DOR expression. Cobalt and nickel, but not zinc, significantly increased DOR expression. Heme synthesis inhibitors would block the synthesis of cobalt-substituted heme proteins which are locked in a deoxygenated conformation. The cobalt-induced increase in DOR expression was blocked by the heme synthesis inhibitor, 4,6-dioxoheptanoic acid. These experiments indicate that deoxygenated conformation heme proteins, which are thought to partially mimic hypoxia, increase DOR expression. The increase in DOR expression suggests that the DOR gene may be hypoxia-sensitive. Further, the increase in DOR expression suggests a potential adaptation strategy to hypoxia and may represent one of the first findings of physiological regulation of DOR expression.

AB - Adaptations to prolonged hypoxia include an increase in the expression of proteins that may facilitate survival. One mechanism by which hypoxia increases protein expression involves a change of heme proteins from oxygenated to deoxygenated conformations. In the present study, we tested the hypothesis that treatment of NG108-15 cells with metallic cations, which are known to induce a deoxygenated conformation of heme proteins, would increase delta opioid receptor (DOR) expression. Cells were treated with cobalt and nickel, which induce deoxygenated heme protein conformation, or zinc as a control for 48 h prior to quantifying DOR expression. Cobalt and nickel, but not zinc, significantly increased DOR expression. Heme synthesis inhibitors would block the synthesis of cobalt-substituted heme proteins which are locked in a deoxygenated conformation. The cobalt-induced increase in DOR expression was blocked by the heme synthesis inhibitor, 4,6-dioxoheptanoic acid. These experiments indicate that deoxygenated conformation heme proteins, which are thought to partially mimic hypoxia, increase DOR expression. The increase in DOR expression suggests that the DOR gene may be hypoxia-sensitive. Further, the increase in DOR expression suggests a potential adaptation strategy to hypoxia and may represent one of the first findings of physiological regulation of DOR expression.

KW - 4,6-Dioxoheptanoic acid

KW - Cobalt

KW - Heme protein

KW - Hypoxia

KW - Naltrindole

KW - NG108-15 cell

KW - δ Opioid receptor

UR - http://www.scopus.com/inward/record.url?scp=0028932533&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028932533&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(95)00089-9

DO - 10.1016/0006-8993(95)00089-9

M3 - Article

C2 - 7614006

AN - SCOPUS:0028932533

VL - 676

SP - 358

EP - 362

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -