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Inhibition of gastrin gene expression by somatostatin
P S Karnik1, S J Monahan, M M Wolfe
1Harvard Digestive Diseases Center, Harvard-Thorndike Laboratory, Boston, Massachusetts.
The Journal of Clinical Investigation
|February 1, 1989
Summary
Somatostatin inhibits gastrin cell function by reducing gastrin messenger RNA (mRNA) levels, affecting gene transcription and potentially mRNA processing. This regulation occurs at the pretranslational level in the antral mucosa.
Area of Science:
- Gastroenterology
- Molecular Endocrinology
- Cell Biology
Background:
- Somatostatin (SST) locally regulates gastrin (GAS) release from antral G-cells.
- Previous research established SST's influence on GAS peptide release.
Purpose of the Study:
- To investigate if SST's effect on antral G-cells involves pretranslational regulation.
- To determine SST's impact on gastrin mRNA levels and gene transcription.
Main Methods:
- Dot blot and Northern blot hybridization to quantify gastrin mRNA levels.
- Nuclear run-off assays to assess gastrin gene transcription rates.
- Use of somatostatin and somatostatin antibodies in incubation studies.
Main Results:
- Somatostatin significantly inhibited steady-state gastrin mRNA levels in a dose-dependent manner.
- Neutralization of somatostatin increased gastrin mRNA levels by 116%.
- Somatostatin antibodies increased gastrin gene transcription by 33.8%, indicating transcriptional inhibition by SST.
Conclusions:
- Somatostatin exerts inhibitory effects on antral gastrin cells at the pretranslational level.
- This inhibition occurs partly at the gene transcriptional level.
- Somatostatin may also influence posttranscriptional processing of gastrin mRNA.
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