The effect of relaxin on the oxytocin receptor in human uterine smooth muscle cells

Ulrike Friebe-Hoffmann, Dunja M. Baston, Jye Ping Chiao, Liza D. Winebrenner, Jan S. Krüssel, Thomas K. Hoffmann, Jens Hirchenhain, Phillip N. Rauk

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Experimental objectives: Activation of the oxytocin receptor (OTR) induces phospholipase C induced PIP2 turnover in the human uterus. Relaxin (RLX), a polypeptide hormone produced in the corpus luteum of pregnancy as well as in the placenta and decidua inhibits PIP2 turnover and subsequent signaling in human myometrium. The purpose of this study was to evaluate a possible effect of RLX on OTR regulation in human uterine smooth muscle cells. Primary cultures of myometrium from term pregnant women undergoing elective caesarean section were incubated for different time periods (0-96 h) and with different concentrations of RLX [10 pg/ml-20 μg/ml]. The effects on OTR binding, mRNA and protein expression were evaluated by means of 125I-OVT binding assay, RT-PCR and flow cytometry. Results: Prolonged RLX incubation was able to inhibit 30-40% of OTR binding while binding affinity remained unchanged. Oxytocin receptor mRNA and protein expression were down regulated by RLX about 50% and 35% respectively. Conclusion: We report for the first time an effect of RLX on OTR regulation in human uterine myometrial cells. The above results indicate that high local uterine RLX concentrations may be involved in uterine quiescence during human pregnancy by down regulating the OTR.

Original languageEnglish (US)
Pages (from-to)74-81
Number of pages8
JournalRegulatory Peptides
Volume138
Issue number2-3
DOIs
StatePublished - Feb 1 2007

Bibliographical note

Funding Information:
U. Friebe‐Hoffmann a was recipient of a scholarship from the German Research Foundation (DFG Fr 1402/1–1) and the Magee‐Women's Research Institute.

Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.

Keywords

  • Insulin-like growth factor family
  • Peptide regulation
  • Preterm labor
  • Signaling

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