Skip to main content
Advertisement

Main menu

  • Home
  • Articles
    • Current Issue
    • Fast Forward
    • Latest Articles
    • Special Sections
    • Archive
  • Information
    • Instructions to Authors
    • Submit a Manuscript
    • FAQs
    • For Subscribers
    • Terms & Conditions of Use
    • Permissions
  • Editorial Board
  • Alerts
    • Alerts
    • RSS Feeds
  • Virtual Issues
  • Feedback
  • Submit
  • Other Publications
    • Drug Metabolism and Disposition
    • Journal of Pharmacology and Experimental Therapeutics
    • Molecular Pharmacology
    • Pharmacological Reviews
    • Pharmacology Research & Perspectives
    • ASPET

User menu

  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
Molecular Pharmacology
  • Other Publications
    • Drug Metabolism and Disposition
    • Journal of Pharmacology and Experimental Therapeutics
    • Molecular Pharmacology
    • Pharmacological Reviews
    • Pharmacology Research & Perspectives
    • ASPET
  • My alerts
  • Log in
  • My Cart
Molecular Pharmacology

Advanced Search

  • Home
  • Articles
    • Current Issue
    • Fast Forward
    • Latest Articles
    • Special Sections
    • Archive
  • Information
    • Instructions to Authors
    • Submit a Manuscript
    • FAQs
    • For Subscribers
    • Terms & Conditions of Use
    • Permissions
  • Editorial Board
  • Alerts
    • Alerts
    • RSS Feeds
  • Virtual Issues
  • Feedback
  • Submit
  • Visit molpharm on Facebook
  • Follow molpharm on Twitter
  • Follow molpharm on LinkedIn
Research ArticleArticle

Agonist Activation of δ-Opioid Receptor but not μ-Opioid Receptor Potentiates Fetal Calf Serum or Tyrosine Kinase Receptor-Mediated Cell Proliferation in a CellLine-Specific Manner

P. Y. Law, T. M. McGinn, K. M. Campbell, L. E. Erickson and H.H. Loh
Molecular Pharmacology January 1997, 51 (1) 152-160; DOI: https://doi.org/10.1124/mol.51.1.152
P. Y. Law
Department of Pharmacology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
T. M. McGinn
Department of Pharmacology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
K. M. Campbell
Department of Pharmacology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
L. E. Erickson
Department of Pharmacology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
H.H. Loh
Department of Pharmacology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Abstract

Activation by opioid receptors of cell proliferation was examined with fibroblast cell lines stably expressing either δ-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 δ-opioid receptor cDNA resulted in an agonist concentration-dependent potentiation of fetal calf serum (FCS)-stimulated cell proliferation. This potentiation by δ-opioid agonists was antagonized by naloxone and was not observed with the κ-opioid receptor selective agonist U50,488 or the μ-opioid receptor selective agonist [d-Ala2,N-MePhe4,Gly-ol5]-enkephalin. This δ-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, δ-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 δ-opioid agonist potentiation of growth apparently was dependent on the level of δ-opioid receptors that were expressed and had cell-line selectivity. Activation of δ-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 δ-opioid receptor cDNA and μ-opioid receptor cDNA, activation of δ- but not μ-opioid receptors resulted in a potentiation of growth. These data suggest that δ- and μ-opioid receptors in CHO cells activate similar but divergent second messenger pathways, resulting in the differential regulation of cell growth.

Footnotes

    • Received September 13, 1995.
    • Accepted September 23, 1996.
  • Send reprint requests to: Dr. Ping Yee Law, Department of Pharmacology, University of Minnesota, 3–249 Millard Hall, 435 Delaware Street, SE, Minneapolis, MN 55455. E-mail:ping{at}lenti.med.umn.edu

  • This research is supported in part by National Institute on Drug Abuse Grants DA07339 and DA05695.

  • The American Society for Pharmacology and Experimental Therapeutics
View Full Text

MolPharm articles become freely available 12 months after publication, and remain freely available for 5 years. 

Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page. 

 

  • Click here for information on institutional subscriptions.
  • Click here for information on individual ASPET membership.

 

Log in using your username and password

Forgot your user name or password?

Purchase access

You may purchase access to this article. This will require you to create an account if you don't already have one.
PreviousNext
Back to top

In this issue

Molecular Pharmacology: 51 (1)
Molecular Pharmacology
Vol. 51, Issue 1
1 Jan 1997
  • Table of Contents
  • About the Cover
  • Index by author
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for sharing this Molecular Pharmacology article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Agonist Activation of δ-Opioid Receptor but not μ-Opioid Receptor Potentiates Fetal Calf Serum or Tyrosine Kinase Receptor-Mediated Cell Proliferation in a CellLine-Specific Manner
(Your Name) has forwarded a page to you from Molecular Pharmacology
(Your Name) thought you would be interested in this article in Molecular Pharmacology.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Research ArticleArticle

Agonist Activation of δ-Opioid Receptor but not μ-Opioid Receptor Potentiates Fetal Calf Serum or Tyrosine Kinase Receptor-Mediated Cell Proliferation in a CellLine-Specific Manner

P. Y. Law, T. M. McGinn, K. M. Campbell, L. E. Erickson and H.H. Loh
Molecular Pharmacology January 1, 1997, 51 (1) 152-160; DOI: https://doi.org/10.1124/mol.51.1.152

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero

Share
Research ArticleArticle

Agonist Activation of δ-Opioid Receptor but not μ-Opioid Receptor Potentiates Fetal Calf Serum or Tyrosine Kinase Receptor-Mediated Cell Proliferation in a CellLine-Specific Manner

P. Y. Law, T. M. McGinn, K. M. Campbell, L. E. Erickson and H.H. Loh
Molecular Pharmacology January 1, 1997, 51 (1) 152-160; DOI: https://doi.org/10.1124/mol.51.1.152
del.icio.us logo Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Experimental Procedures
    • Results
    • Discussion
    • Acknowledgments
    • Footnotes
    • Abbreviations
    • References
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • EIPA, HMA and SMN2 gene regulation
  • Clc-2 has minor role in intestinal Cl- secretion
  • Resveratrol acts as an NR4A1 antagonist in lung cancer.
Show more Article

Similar Articles

Advertisement
  • Home
  • Alerts
Facebook   Twitter   LinkedIn   RSS

Navigate

  • Current Issue
  • Fast Forward by date
  • Fast Forward by section
  • Latest Articles
  • Archive
  • Search for Articles
  • Feedback
  • ASPET

More Information

  • About Molecular Pharmacology
  • Editorial Board
  • Instructions to Authors
  • Submit a Manuscript
  • Customized Alerts
  • RSS Feeds
  • Subscriptions
  • Permissions
  • Terms & Conditions of Use

ASPET's Other Journals

  • Drug Metabolism and Disposition
  • Journal of Pharmacology and Experimental Therapeutics
  • Pharmacological Reviews
  • Pharmacology Research & Perspectives
ISSN 1521-0111 (Online)

Copyright © 2022 by the American Society for Pharmacology and Experimental Therapeutics