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Stromal cell-specif...
Stromal cell-specific apoptotic and antiestrogenic mechanisms may explain uterine defects in humans after clomiphene citrate therapy.
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- Nutu, Magdalena, 1967 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
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- Feng, Yi (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
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- Egecioglu, Emil, 1977 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
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- Weijdegård, Birgitta (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
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- Stener-Victorin, Elisabet, 1964 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi,Institutionen för neurovetenskap och fysiologi,Institute of Clinical Sciences, Department of Obstetrics and Gynecology,Institute of Neuroscience and Physiology
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- Shao, Linus Ruijin, 1964 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
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(creator_code:org_t)
- Elsevier BV, 2010
- 2010
- Engelska.
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Ingår i: American journal of obstetrics and gynecology. - : Elsevier BV. - 1097-6868 .- 0002-9378. ; 203:1
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https://gup.ub.gu.se...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- OBJECTIVE: The purpose of this study was to investigate clomiphene citrate (CC)-induced modulation of uterine cell function in vivo. STUDY DESIGN: Prepubertal female Sprague-Dawley rats were treated intraperitoneally with CC for 6 or 24 hours or with a combination of CC and/or 17-beta-estradiol (E2) for 4 days. RESULTS: Chronic CC treatment induced apoptosis in a fraction of uterine stromal cells by activating the caspase-3-mediated apoptotic pathway. The damage was prevented by successive E2 treatment; however, pretreatment or concomitant treatment with E2 did not protect against CC-induced uterine apoptosis. CC decreased the protein expression of estrogen receptor alpha and increased its phosphorylation but did not affect estrogen receptor beta expression or phosphorylation. Furthermore, changes in Hoxa11, p27, and progesterone receptor protein levels and localization were associated with CC treatment. CONCLUSION: We provide novel mechanistic insights into cellular and molecular events by which CC regulates uterine stromal cell function and hence the implantation process and pregnancy outcome.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Physiology (hsv//eng)
Nyckelord
- Animals
- Apoptosis
- drug effects
- physiology
- Caspase 3
- metabolism
- Clomiphene
- pharmacology
- Estradiol
- pharmacology
- Estrogen Receptor alpha
- metabolism
- Estrogen Receptor beta
- biosynthesis
- metabolism
- Female
- Immunohistochemistry
- In Situ Hybridization
- Fluorescence
- Microscopy
- Immunoelectron
- Random Allocation
- Rats
- Rats
- Sprague-Dawley
- Selective Estrogen Receptor Modulators
- pharmacology
- Signal Transduction
- Stromal Cells
- drug effects
- metabolism
- pathology
- Uterus
- drug effects
- metabolism
- pathology
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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