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Tamoxifen-Mediated Changes in Estrogen-Dependent Gene Expression in Hypothalamic Neurons Responsible for Hot Flashes.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Tamoxifen-Mediated Changes in Estrogen-Dependent Gene Expression in Hypothalamic Neurons Responsible for Hot Flashes./
Author:	Misquez, Amanda Marie.
Description:	1 online resource (62 pages)
Notes:	Source: Masters Abstracts International, Volume: 84-12.
Contained By:	Masters Abstracts International84-12.
Subject:	Physiology. -
Online resource:	click for full text (PQDT)
ISBN:	9798379719524

Tamoxifen-Mediated Changes in Estrogen-Dependent Gene Expression in Hypothalamic Neurons Responsible for Hot Flashes.
Misquez, Amanda Marie.

Tamoxifen-Mediated Changes in Estrogen-Dependent Gene Expression in Hypothalamic Neurons Responsible for Hot Flashes. - 1 online resource (62 pages)

Source: Masters Abstracts International, Volume: 84-12.

Thesis (M.S.)--University of California, Los Angeles, 2023.

Includes bibliographical references

Tamoxifen (Tmx) is a selective estrogen receptor modulator widely used as a chemotherapeutic drug in the treatment regimen for estrogen-sensitive breast cancer. Tmx treatment leads to many side effects; the most prominently reported side effect is hot flashes. Hot flashes are episodes of thermodysregulation and have been shown to be caused by estrogen-receptor α (ERα) signaling in the hypothalamus. In this thesis, we delivered a custom, bi-functional fluorescent reporter to three estrogen-sensitive nuclei in the hypothalamus that regulate body temperature: the medial preoptic area (MPA), the arcuate nucleus (ARC), and the ventrolateral region of the ventromedial hypothalamus (VMHvl). The reporter labels estrogen-sensitive neurons that express ERα and reports whether neurons alter estrogen-dependent gene transcription and expression in response to Tmx treatment. Upon delivering the fluorescent reporter to the three thermoregulatory and estrogen-sensitive regions of interest (the MPA, ARC, and VMHvl), we observed that Tmx treatment in Esr1 Cre and Kiss1 Cre mice showed no significant differences in ERE-dependent gene expression in the MPA, ARC, and VMHvl compared to control, Oil-treated mice. Therefore, we are unable to detect Tmx-induced changes in gene expression in estrogen-sensitive neurons of the MPA, ARC, or VMHvl. We conclude that Tmx does not alter estrogen-dependent gene expression in the hypothalamus under the conditions we used. As our Tamoxifen treatment paradigm is sufficient to induce thermodysregulation, this implies the intriguing possibility that Tamoxifen induces hot flashes without widespread changes in hypothalamic gene expression.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798379719524Subjects--Topical Terms:

673386
Physiology.
Subjects--Index Terms:

Arcuate nucleusIndex Terms--Genre/Form:

554714
Electronic books.

Tamoxifen-Mediated Changes in Estrogen-Dependent Gene Expression in Hypothalamic Neurons Responsible for Hot Flashes.
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520 $a Tamoxifen (Tmx) is a selective estrogen receptor modulator widely used as a chemotherapeutic drug in the treatment regimen for estrogen-sensitive breast cancer. Tmx treatment leads to many side effects; the most prominently reported side effect is hot flashes. Hot flashes are episodes of thermodysregulation and have been shown to be caused by estrogen-receptor α (ERα) signaling in the hypothalamus. In this thesis, we delivered a custom, bi-functional fluorescent reporter to three estrogen-sensitive nuclei in the hypothalamus that regulate body temperature: the medial preoptic area (MPA), the arcuate nucleus (ARC), and the ventrolateral region of the ventromedial hypothalamus (VMHvl). The reporter labels estrogen-sensitive neurons that express ERα and reports whether neurons alter estrogen-dependent gene transcription and expression in response to Tmx treatment. Upon delivering the fluorescent reporter to the three thermoregulatory and estrogen-sensitive regions of interest (the MPA, ARC, and VMHvl), we observed that Tmx treatment in Esr1 Cre and Kiss1 Cre mice showed no significant differences in ERE-dependent gene expression in the MPA, ARC, and VMHvl compared to control, Oil-treated mice. Therefore, we are unable to detect Tmx-induced changes in gene expression in estrogen-sensitive neurons of the MPA, ARC, or VMHvl. We conclude that Tmx does not alter estrogen-dependent gene expression in the hypothalamus under the conditions we used. As our Tamoxifen treatment paradigm is sufficient to induce thermodysregulation, this implies the intriguing possibility that Tamoxifen induces hot flashes without widespread changes in hypothalamic gene expression.
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