Tissue-Protective Effects of Estrogen Involve Regulation of Caspase Gene Expression

Monroe, David G.; Berger, Ryan R.; Sanders, Michel M.

doi:10.1210/mend.16.6.0855

Cited by 55 publications

(38 citation statements)

References 44 publications

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“…There is evidence that the presence of estrogen protects cells from apoptosis, whereas withdrawal of estrogen induces apoptosis (29,30). Indirectly, our data are consistent with the above reports.…”

Section: Discussionsupporting

confidence: 93%

Expression of Metabolic and Apoptotic Genes During Treatment With Chemopreventive Agents for Breast Cancer

Lu¹

2005

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Section: Discussionsupporting

confidence: 93%

Expression of Metabolic and Apoptotic Genes During Treatment With Chemopreventive Agents for Breast Cancer

Lu¹

2005

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“…In addition to its mitogenic effects, E is also known to promote cell survival by acting as an antiapoptotic agent (31,52). A block in E-induced uterine LE cell proliferation in the absence of C/EBP␤ may trigger apoptosis, which is the culmination of a cascade of molecular steps, including cell cycle withdrawal and DNA fragmentation (27).…”

Section: Discussionmentioning

confidence: 99%

Lack of CCAAT Enhancer Binding Protein Beta (C/EBPβ) in Uterine Epithelial Cells Impairs Estrogen-Induced DNA Replication, Induces DNA Damage Response Pathways, and Promotes Apoptosis

Ramathal

Bagchi

2010

Molecular and Cellular Biology

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Female mice lacking the transcription factor C/EBP␤ are infertile and display markedly reduced estrogen (E)-induced proliferation of the uterine epithelial lining during the reproductive cycle. The present study showed that E-stimulated luminal epithelial cells of a C/EBP␤-null uterus are able to proceed through the G 1 phase of the cell cycle before getting arrested in the S phase. This cell cycle arrest was accompanied by markedly reduced levels of expression of E2F3, an E2F family member, and a lack of nuclear localization of cyclin E, a critical regulator of cdk2. An increased nuclear accumulation of p27, an inhibitor of the cyclin E-cdk2 complex, was also observed for the mutant epithelium. Gene expression profiling of C/EBP␤-null uterine epithelial cells revealed that the blockade of E-induced DNA replication triggers the activation of several well-known components of the DNA damage response pathway, such as ATM, ATR, histone H2AX, checkpoint kinase 1, and tumor suppressor p53. The activation of p53 by ATM/ATR kinase led to increased levels of expression of p21, an inhibitor of G 1 -S-phase progression, which helps maintain cell cycle arrest. Additionally, p53-dependent mechanisms contributed to an increased apoptosis of replication-defective cells in the C/EBP␤-null epithelium. C/EBP␤, therefore, is an essential mediator of E-induced growth and survival of uterine epithelial cells of cycling mice.The ovarian steroid hormones estrogen (E) and progesterone (P) play critical roles in the maintenance of the mammalian uterus through cyclical rounds of cell proliferation and differentiation during the reproductive cycle (50). In rodents, ovarian E produced during the proestrus stage stimulates uterine luminal and glandular epithelial cell proliferation, preparing the uterus for potential pregnancy. During this growth phase, E causes distinct physiological changes such as an increased uterine wet weight and structural remodeling of the luminal epithelium (LE) cell layer while also accelerating their entry into the S phase of the cell cycle (17,18,29,50). At the onset of pregnancy, increasing levels of P produced from the newly formed corpora lutea in the ovaries suppresses the Estimulated proliferation of uterine LE cells. The actions of E and P in these epithelial cells are mediated via their respective nuclear receptors, estrogen receptor alpha (ER␣) and progesterone receptor (PR) (23, 26). Acting in concert, these hormones control early events that are essential for providing a suitable environment for blastocyst attachment to LE cells and successful implantation. In the adult female mouse, the administration of exogenous E and P to ovariectomized mice faithfully reproduces the uterine epithelial responses seen during the estrous cycle and early pregnancy. Therefore, mouse uterine LE cells offer an excellent model with which one may explore the molecular mechanisms by which steroid hormones control cell proliferation.Several previous studies documented the mitogenic effects of E on rodent uterine LE cells and...

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“…Studies in chick oviduct confirm our results for Bcl-2. Monroe et al (11) found that the expression of Bcl-2 remained constant in the chick oviduct with exposure and removal of estradiol in culture.…”

Section: Discussionmentioning

confidence: 99%

Changes in the ratio of Bax and Bcl-2 mRNA expression and their cellular localization throughout the ovulatory cycle in the human oviduct

Briton-Jones

Lok

et al. 2006

J Assist Reprod Genet

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Purpose: To examine changes in the ratio of Bax and Bcl-2 mRNA expression throughout the ovulatory cycle in the ampullary region of the human oviduct. Methods: The mucosal layer was isolated from the human oviduct tissue and semiquantitative reverse-transcriptase polymerase chain-reaction (RT-PCR) analysis of mRNA of Bax and Bcl-2 was performed. Immunohistochemistry provided the cellular localization of the Bax and Bcl-2 proteins. The ratio of expression of Bax and Bcl-2 mRNA was examined in the ampullary region of the oviduct in samples obtained in the follicular, periovulatory, and luteal phases of the ovulatory cycle. Results: Bax expression was constant in the follicular and periovulatory phase but showed a significant increase in the luteal phase. The Bax protein was present in all oviduct mucosal epithelial cells and the intensity of staining increased in luteal phase samples. Bcl-2 was expressed at a relatively constant level throughout the ovulatory cycle. The Bcl-2 protein was present in some but not all mucosal epithelial cells and the proportion of positive cells remained constant throughout the ovulatory cycle. Conclusion:The proapoptotic gene Bax shows a significant increase in mRNA expression in the luteal phase of the ovulatory cycle while the expression level of the antiapoptotic gene Bcl-2 remains constant throughout the ovulatory cycle. The ratio of Bax:Bcl-2 increases significantly in the luteal phase consistent with cells undergoing apoptosis.

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Tissue-Protective Effects of Estrogen Involve Regulation of Caspase Gene Expression

Cited by 55 publications

References 44 publications

Expression of Metabolic and Apoptotic Genes During Treatment With Chemopreventive Agents for Breast Cancer

Expression of Metabolic and Apoptotic Genes During Treatment With Chemopreventive Agents for Breast Cancer

Lack of CCAAT Enhancer Binding Protein Beta (C/EBPβ) in Uterine Epithelial Cells Impairs Estrogen-Induced DNA Replication, Induces DNA Damage Response Pathways, and Promotes Apoptosis

Changes in the ratio of Bax and Bcl-2 mRNA expression and their cellular localization throughout the ovulatory cycle in the human oviduct

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