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Ectopic serotonin production in β-cell specific transgenic mice.
Hyeongseok Kim1, Hyunki Kim1, Kyuho Kim1
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 34141, Republic of Korea.
Biochemical and Biophysical Research Communications
|December 11, 2017
Summary
Transgenic mice with human growth hormone (hGH) cassettes may exhibit ectopic serotonin production in pancreatic beta cells. This is due to hGH activating the prolactin receptor-Stat5-Tph1 pathway, confounding research results.
Area of Science:
- Endocrinology
- Molecular Biology
- Genetics
Background:
- Genetically modified mice are crucial tools in beta-cell research.
- Interpreting data from these models requires careful consideration of potential confounding factors.
Purpose of the Study:
- To investigate the phenomenon of ectopic serotonin (5-HT) production in beta cells of specific transgenic mouse models.
- To elucidate the molecular mechanisms underlying this ectopic 5-HT production.
Main Methods:
- Analysis of beta cells in RIP-CreMgn, MIP-GFP, and MIP-Cre/ERT transgenic mice.
- Assessment of human growth hormone (hGH) cassette effects on transgene expression and pathway activation.
- Investigation using beta-cell-specific prolactin receptor (Prlr) and Stat5 knockout mouse models.
Main Results:
- Ectopic serotonin (5-HT) production was observed in beta cells of transgenic mice carrying an hGH cassette.
- Tryptophan hydroxylase 1 (Tph1) expression was upregulated in islets of transgenic mice with the hGH cassette.
- The Prlr-Stat5-Tph1 pathway was identified as the mechanism driving hGH-induced 5-HT production in beta cells.
Conclusions:
- The presence of an hGH cassette in transgenic mice can lead to confounding results due to ectopic serotonin production in beta cells.
- Researchers using these transgenic models must account for the influence of the hGH cassette and the Prlr-Stat5-Tph1 pathway.
