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-Opioid Receptor but not µ-Opioid
Receptor Potentiates Fetal Calf Serum or Tyrosine Kinase
Receptor-Mediated Cell Proliferation in a CellLine-Specific Manner
Department of Pharmacology, Medical School, University of
Minnesota, Minneapolis, Minnesota 55455
Activation by opioid receptors of cell proliferation was examined with
fibroblast cell lines stably expressing either 
-opioid or µ-opioid
receptors. Addition of
[D-Ala2,D-Leu5]-enkephalin
or
[D-Pen2,D-Pen5]-enkephalin
to Chinese hamster ovary (CHO) cells transfected with -opioid
receptor cDNA resulted in an agonist concentration-dependent potentiation of fetal calf serum (FCS)-stimulated cell proliferation. This potentiation by -opioid agonists was antagonized by naloxone and was not observed with the 
-opioid receptor selective agonist U50,488 or the µ-opioid receptor selective agonist
[D-Ala2,N-MePhe4,Gly-ol5]-enkephalin.
This -opioid agonist effect was not observed at FCS concentrations
>0.1% and could be blocked by pretreating cells with pertussis toxin,
indicating that Gi/Go were involved in this action. In addition, -opioid agonists could potentiate CHO cell proliferation stimulated by those growth factors that are mediated by
tyrosine kinase receptors (i.e., insulin, insulin-like growth factor 1, and fibroblast-derived growth factor b). This -opioid agonist
potentiation of growth apparently was dependent on the level of
-opioid receptors that were expressed and had cell-line selectivity.
Activation of -opioid receptors expressed in Rat-1 or NIH3T3
fibroblast did not result in a modulation of the cell growth induced by
FCS or by growth factors. Interestingly, in CHO cells transfected with
µ-opioid receptor cDNA, activation with agonists did not produce a
potentiation of FCS-stimulated proliferation. This lack of µ-opioid
receptor effect was not due to the differences among CHO clones. In a
CHO cell line transfected with both -opioid receptor cDNA and
µ-opioid receptor cDNA, activation of - but not µ-opioid
receptors resulted in a potentiation of growth. These data suggest that
- and µ-opioid receptors in CHO cells activate similar but
divergent second messenger pathways, resulting in the differential
regulation of cell growth.
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