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17beta-estradiol stimulates substance P receptor gene expression
1Department of Internal Medicine, University of California, Davis 95616, USA. avillablanca@ucdavis.edu
Molecular and Cellular Endocrinology
|March 4, 1998
Summary
Hormonal regulation of the substance P receptor (SPR) was investigated. 17beta-estradiol significantly increased SPR mRNA levels in a time- and concentration-dependent manner, suggesting hormonal control over receptor gene expression.
Area of Science:
- Neuroendocrinology
- Molecular Biology
- Cell Biology
Background:
- Substance P (SP) is a neuropeptide regulating cellular functions via the NK1 receptor.
- Sexual dimorphism in SP and SPR expression suggests hormonal influence.
- AR42J cells express high levels of the SP receptor (SPR).
Purpose of the Study:
- To investigate the effect of 17beta-estradiol (E2) on SPR gene expression.
- To explore the molecular mechanisms of hormonal control on SPR.
Main Methods:
- Northern blot analysis to quantify SPR mRNA levels.
- Treatment with 17beta-estradiol (E2), actinomycin D, and tamoxifen.
- Measurement of [3H]SP binding to SPR.
Main Results:
- 17beta-estradiol (100 nM) increased SPR mRNA by 2.5-fold.
- The E2 effect was time- and concentration-dependent and required RNA transcription.
- Tamoxifen blocked the stimulatory effect of E2, and increased mRNA correlated with increased SP binding.
Conclusions:
- 17beta-estradiol upregulates SPR gene expression in AR42J cells.
- Hormonal control of SPR expression involves transcriptional regulation.
- Findings provide insight into the molecular mechanisms of hormonal regulation of receptor gene expression.