Mini-review: estrogen action in the uterus and insulin-like growth factor-I

Moyano, Paula; Rotwein, Peter

doi:10.1016/j.ghir.2004.09.001

Cited by 25 publications

(18 citation statements)

References 58 publications

(78 reference statements)

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“…The growth hormone signaling activated transcription factor, STAT5, is also a regulator of Igf1 transcript levels in the rodent liver via interaction with growth hormone-responsive element (GHRE) sites in the Igf1 gene (17,18). The rodent uterus contains STAT5 protein as well, and in this study we observed a WT ER␣-dependent increase in Stat5a transcript.…”

supporting

confidence: 51%

“…Igf1 Is Not Increased by E 2 in the KIKO-Igf1 is critical to the uterine growth responses (12,13,17), and the Igf1 transcript is reported to be an example of a gene response mediated by the tethered ER␣ mechanism, where ER␣ indirectly interacts with other transcription factors on promoter sequences rather than directly binding to DNA (16). Surprisingly, no increase in the Igf1 transcript was seen in the KIKO mouse uterus, which has a mutation in the ER␣, rendering it unable to bind directly to ERE sequences, but selectively preserves its ability to interact with other transcription factors (5,6).…”

Section: Resultsmentioning

confidence: 99%

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Estrogen-mediated Regulation of Igf1 Transcription and Uterine Growth Involves Direct Binding of Estrogen Receptor α to Estrogen-responsive Elements

Hewitt

Yin

et al. 2010

Journal of Biological Chemistry

109

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Estrogen enables uterine proliferation, which depends on synthesis of the IGF1 growth factor. This proliferation and IGF1 synthesis requires the estrogen receptor (ER), which binds directly to target DNA sequences (estrogen-responsive elements or EREs), or interacts with other transcription factors, such as AP1, to impact transcription. We observe neither uterine growth nor an increase in Igf1 transcript in a mouse with a DNA-binding mutated ER␣ (KIKO), indicating that both Igf1 regulation and uterine proliferation require the DNA binding function of the ER. We identified several potential EREs in the Igf1 gene, and chromatin immunoprecipitation analysis revealed ER␣ binding to these EREs in wild type but not KIKO chromatin. STAT5 is also reported to regulate Igf1; uterine Stat5a transcript is increased by estradiol (E 2 ), but not in KIKO or ␣ERKO uteri, indicating ER␣-and ERE-dependent regulation. ER␣ binds to a potential Stat5a ERE. We hypothesize that E 2 increases Stat5a transcript through ERE binding; that ER␣, either alone or together with STAT5, then acts to increase Igf1 transcription; and that the resulting lack of IGF1 impairs KIKO uterine growth. Treatment with exogenous IGF1, alone or in combination with E 2 , induces proliferation in wild type but not KIKO uteri, indicating that IGF1 replacement does not rescue the KIKO proliferative response. Together, these observations suggest in contrast to previous in vitro studies of IGF-1 regulation involving AP1 motifs that direct ER␣-DNA interaction is required to increase Igf1 transcription. Additionally, full ER␣ function is needed to mediate other cellular signals of the growth factor for uterine growth.

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supporting

confidence: 51%

Section: Resultsmentioning

confidence: 99%

Estrogen-mediated Regulation of Igf1 Transcription and Uterine Growth Involves Direct Binding of Estrogen Receptor α to Estrogen-responsive Elements

Hewitt

Yin

et al. 2010

Journal of Biological Chemistry

109

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“…Myszy pozbawione genu kodującego IGF-I wykazywały znaczną hipoplazję macicy. Niedostępność IGF-I w macicy spowodowała, że samice były niepłodne, nie przejawiając cykli płciowych nawet po stymulacji gonadotropinami (44). Natomiast u szczurów, u których przeprowadzono zabieg usunięcia jajników, podanie egzogennego IGF-I powodowało rozrost endometrium (10).…”

Section: Czynnik Wzrostu śRódbłonka Naczyniowego (Vascular Endotheliaunclassified

“…(43) podczas analiz immunohistochemicznych wykazali, iż ekspresja IGF-I w macicy szczurów podczas cyklu płciowego i wczesnej ciąży zależna jest od dostępności E2 oraz P4. Podczas cyklu płciowego u kobiet, IGF-I pośredniczy w zależnej od estrogenu rozbudowie endometrium podczas fazy proliferacyjnej, natomiast podczas fazy wydzielniczej odnotowano udział IGF-II w powiązaniu z progesteronem (44,48,52). Ponadto, obie izoformy IGF wykazują mitogenne działanie w doczesnych komórkach zrębu endometrium (24,52).…”

Section: Czynnik Wzrostu śRódbłonka Naczyniowego (Vascular Endotheliaunclassified

Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system

Woźna¹,

Rybska²,

Swierczewska³

et al. 2017

Medycyna Weterynaryjna

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*) Projekt został sfinansowany ze środków Narodowego Centrum Nauki przyznanych na podstawie decyzji DEC-2013/09/N/NZ5/0183. Woźna M., Rybska M., Świerczewska M., Jaśkowski J. M.Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system Summary The endometrium of the uterus is a highly dynamic structure in terms of its changes during the various stages of the sexual cycle. These changes are the result of cyclical fluctuations in the concentrations of steroid hormones and local factors of an auto -and paracrine -nature. This condition indicates that the causes of degenerative processes of the uterus must be sought not only in disorders of the hormonal profile and bacterial infections but also disorders at the molecular level. Factors that may play a key role in the formation and development of various pathologies of the female reproductive system include growth factors and their receptors (growth factors -GFs). Discussing these growth factors in the work may provide useful molecular markers that identify pathological conditions of the endometrium. Subject to expression in the endometrium, they are involved in the regulation of cell proliferation, migration and secretion of the glandular epithelium, they also regulate physiological and pathological angiogenesis, revealing strong pro-inflammatory effects. In this research, the authors present an overview of current scientific reports indicating that changes in the expression of studied factors, and thus disturbances in their effects, may constitute one of the causes of pathogenesis within the uterus in many animal species.

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“…There is evidence suggesting that IGF-I acts as a mediator of E 2 within the uterus. Mice lacking IGF-I are infertile and have underdeveloped uteri similar to that of mice lacking ERα [62]. Similar to EGFR in breast cancer cells, increased IGF-IR has been demonstrated following E 2 treatment, thus sensitizing the breast cancer cells to 11 IGF-I activity [58].…”

Section: Insulin-like Growth Factor-imentioning

confidence: 99%

Innate Immunity in the Female Reproductive Tract: Role of Sex Hormones in Regulating Uterine Epithelial Cell Protection Against Pathogens

Ochiel

Fahey²,

Ghosh³

et al. 2008

CWHR

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The mucosal immune system in the upper female reproductive tract is uniquely prepared to maintain a balance between the presence of commensal bacteria, sexually transmitted bacterial and viral pathogens, allogeneic spermatozoa, and an immunologically distinct fetus. At the center of this dynamic system are the epithelial cells that line the Fallopian tubes, uterus, cervix and vagina. Epithelial cells provide a first line of defense that confers continuous protection, by providing a physical barrier as well as secretions containing bactericidal and virucidal agents. In addition to maintaining a state of ongoing protection, these cells have evolved to respond to pathogens, in part through Toll-like receptors (TLRs), to enhance innate immune protection and, when necessary, to contribute to the initiation of an adaptive immune response. Against this backdrop, epithelial cell innate and adaptive immune function is modulated to meet the constraints of procreation. The overall goal of this review is to focus on the dynamic role of epithelial cells in the upper reproductive tract, with special emphasis on the uterus, to define the unique properties of these cells as they maintain homeostasis in preparation for successful fertilization and pregnancy while at the same time confer protection against sexually transmitted infections, which threaten to compromise women's reproductive health and survival. By understanding the nature of this protection and the ways in which innate and adaptive immunity are regulated by sex hormones, these studies provide the opportunity to contribute to the foundation of information essential for ensuring reproductive health.

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Mini-review: estrogen action in the uterus and insulin-like growth factor-I

Cited by 25 publications

References 58 publications

Estrogen-mediated Regulation of Igf1 Transcription and Uterine Growth Involves Direct Binding of Estrogen Receptor α to Estrogen-responsive Elements

Estrogen-mediated Regulation of Igf1 Transcription and Uterine Growth Involves Direct Binding of Estrogen Receptor α to Estrogen-responsive Elements

Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system

Innate Immunity in the Female Reproductive Tract: Role of Sex Hormones in Regulating Uterine Epithelial Cell Protection Against Pathogens

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