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Cited by 54Endometriosis Research and TreatmentEstrogen and related hormone effectsEctopic Pregnancy Diagnosis and Management

Treatment with Bazedoxifene and Conjugated Estrogens Results in Regression of Endometriosis in a Murine Model1

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Naqvi, Hanyia, Sakr, Sharif, Presti, Thomas, Krikun, Graciela, Komm, Barry, Taylor, Hugh S.·2014·Biology of Reproduction
DOI 10.1095/biolreprod.113.114165PMC PMC4093999
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Abstract

Bazedoxifene (BZA), a selective estrogen receptor modulator (SERM), inhibits the action of estrogens on endometrial proliferation. Here, we evaluate the effect of a tissue-selective estrogen complex (TSEC) containing BZA and conjugated estrogens (CE) on ectopic endometrial lesions in a mouse model of endometriosis. Experimental endometriosis was created in 60 female CD-1 mice. The mice were randomly divided into 10 groups that received varying doses of either BZA (1, 2, 3, or 5 mg/kg/day), BZA (1, 2, 3, or 5 mg/kg/day) in combination with CE (3 mg/kg/day), CE treatment alone (3 mg/kg/day), or vehicle control for 8 wk. Treatment with BZA alone or the TSEC containing BZA/CE led to a decrease in endometriotic lesion size compared to controls. The mean surface area of the untreated lesions was 19.6 mm(2). Treatment with BZA or BZA/CE resulted in reduced lesion size (to 8.8 and 7.8 mm(2), respectively). No significant difference was found in lesion size between the BZA and BZA/CE treatment groups or between different doses of either treatment. Ovarian cyst formation was not evident in the treated groups. Treatment with the TSEC containing higher BZA dosages (3 and 5 mg/kg/day) led to significantly lower levels of estrogen receptor (Esr1) mRNA expression compared to the control treatment. No differences were observed in expression of progesterone receptor (Pgr). Immunohistochemical analysis also demonstrated a decrease in ESR protein. The combination of CE and BZA may prove to be a novel treatment option for endometriosis.

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  • Raloxifene and bazedoxifene both result in lesion regression and inhibition of proliferation in murine models.

    “Raloxifene and bazedoxifene both result in lesion regression and inhibition of proliferation in murine models (Yao et al., 2005;Kulak et al., 2011;Naqvi et al., 2014).”

    From Endometriosis and nuclear receptors (2019) · cites this paper as Naqvi et al., 2014

    The Results (page unavailable) show that bazedoxifene, alone or with conjugated estrogens, reduced endometriotic lesion size in mice. The Discussion (page unavailable) presents inhibition of endometrial proliferation as a suggested mechanism, not a directly established result. This paper does not establish the raloxifene portion of the sentence, which is also cited to other studies. (LLM, conf=0.86)

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  • While ESR2 mediates estradiol-dependent anti-apoptosis and proliferation in human lesions, its expression is variable in murine models of endometriosis with ESR1 dominancy in most models.

    “First, while ESR2 mediates estradiol-dependent anti-apoptosis and proliferation in human lesions, its expression is variable in murine models of endometriosis with ESR1 dominancy in most models (Kulak et al., 2011;Naqvi et al., 2014).”

    From Endometriosis and nuclear receptors (2019) · cites this paper as Naqvi et al., 2014

    The Results and Discussion (page unavailable) show that ESR1 expression in this murine model changes with treatment and suggest ESR1 contributes to endometrial proliferation. The paper does not establish variable ESR2 expression or ESR1 dominance across most murine models, nor does it address ESR2-mediated anti-apoptosis and proliferation in human lesions. (LLM, conf=0.78)

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1 of the 51 references couldn’t be matched to a known paper.

Research works printed but not linked: 4

  1. Giudice LC, Kao LC. Endometriosis. Lancet 2004; 364(9447):1789-1799.
  2. Bulun SE. Endometriosis. N Engl J Med 2009; 360(3):268-279.
  3. Olive DL, Pritts EA. Treatment of endometriosis. N Engl J Med 2001; 345(4):266-275.
  4. Vercellini P, Somigliana E, Vigano `P, Abbiati A, Barbara G, Crosignani PG. Endometriosis. Drugs 2009; 69(6):649-675.

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Authors
Naqvi, H., Sakr, S., Presti, T., Krikun, G., Komm, B., & Taylor, H. S.
Affiliations
  • Yale University (US)
  • Pfizer (United States) (US)
Corresponding author
Taylor, Hugh S.
ORCID
Venue
Biology of Reproduction
Publisher
Oxford University Press (OUP)
Published
2014-06-01
Volume
90
Issue
6
Pages
121-121
ISSN
  • 0006-3363 (ISSN-L)
  • 1529-7268
DOI
10.1095/biolreprod.113.114165
PMC
PMC4093999
OpenAlex
W2052516455
Cited by
54
References
51
Citations by year
2026: 2 · 2025: 1 · 2024: 2 · 2022: 6 · 2021: 4 · 2020: 4 · 2019: 6 · 2018: 11 · 2017: 7 · 2016: 3 · 2015: 6 · 2014: 2
FWCI
7.27
Type
journal article
Language
en
Open access
Locations
  • Biology of Reproduction (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • BioOne Complete (BioOne) (submittedVersion)
Topics
  • Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ectopic Pregnancy Diagnosis and Management
Keywords
endometriosis, bazedoxifene, conjugated estrogens, tissue-selective estrogen complex, selective estrogen receptor modulators, estrogen receptor alpha, progesterone receptor, mouse model of endometriosis
MeSH terms
Animals, Disease Models, Animal, Endometriosis, Estrogens, Conjugated (USP), Female, Ovarian Follicle, Humans, Indoles, Mice, Inbred Strains, Organ Size, Random Allocation, Receptors, Progesterone, Treatment Outcome, Selective Estrogen Receptor Modulators, Estrogen Receptor alpha, Cell Proliferation

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