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Detection and Isolation of Apoptotic Bodies to High Purity
Published on: August 12, 2018
Apoptosis in human endometrium: apoptotic detection methods and signaling
1Department of Anatomy and Biology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki, Osaka 569-8686, Japan. an1001@art.osaka-med.ac.jp
Summary
Apoptosis in the human endometrium involves Bcl-2, a protein that blocks cell death during the proliferative phase. During the secretory phase, decreased Bcl-2 and increased caspases promote apoptosis via multiple pathways.
Area of Science:
- Reproductive Biology
- Cellular Biology
- Gynecology
Background:
- Apoptosis is recognized in the human endometrium during the late secretory and menstruating phases.
- The regulation of endometrial apoptosis during the menstrual cycle is not fully elucidated.
Purpose of the Study:
- To investigate the cyclic expression of Bcl-2, Sp-3, c-Jun, Fas, and Fas ligand in human endometrial glandular cells.
- To explore the potential roles of Sp-3 and c-Jun as transcriptional factors for Bcl-2.
- To understand the involvement of mitochondrial and death-receptor pathways in endometrial apoptosis.
Main Methods:
- Analysis of Bcl-2, Sp-3, c-Jun, Fas, and Fas ligand expression throughout the menstrual cycle.
- Assessment of caspase-3, -8, and -9 activities during different phases.
- Correlation of protein expression patterns with apoptotic events.
Main Results:
- Bcl-2 expression peaked in the late proliferative phase and decreased during the secretory phase, coinciding with increased apoptosis.
- Sp-3 and c-Jun expression patterns mirrored Bcl-2, suggesting their role in its transcription.
- Fas and Fas ligand were coexpressed throughout the cycle, with heightened Fas ligand expression in the secretory to menstruating phases.
- Caspase activities were elevated from the secretory to menstruating phases.
Conclusions:
- Bcl-2 transcription, potentially regulated by Sp-3 and c-Jun, is upregulated during the proliferative phase, inhibiting apoptosis.
- During the secretory phase, endometrial glandular cells undergo apoptosis through both death-receptor and mitochondrial pathways, indicated by decreased Bcl-2 and activated caspases.
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