| OESTRADIOL REGULATED PROGRAMMED CELL DEATH IN RAT VAGINA: TERMINAL DIFFERENTIATION OR APOPTOSIS? |
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| 收稿时间： | 25 September 1997 |
OESTRADIOL REGULATED PROGRAMMED CELL DEATH IN RAT VAGINA: TERMINAL DIFFERENTIATION OR APOPTOSIS? |
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| Authors: | K SRIDHAR RAO S ZANOTTI A G REDDY F RAUCH H G MANNHERZ P D GUPTA |
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| Institution: | 1. Menopause Andropause Research Center, Midwifery Department, School of Nursing and Midwifery, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran;2. Department of Midwifery, School of Nursing and Midwifery, Menopause Andropause Research Center, Reproductive Health Promotion Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran;3. Department of Pharmaceutics, School of Pharmacy, Nanotechnology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran;4. Department of Biostatistics and Epidemiology, School of Health, Atherosclerosis Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran |
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| Abstract: | Rat vaginal epithelial cells (VEC) undergo division and differentiation under the influence of oestradiol in a programmed manner. The differentiation process of VEC leads to keratinization, cornification and subsequent desquamation of the dead cells. This process of programmed cell death, referred to as terminal differentiation may share some common pathways with cell death by apoptosis but differ substantially in many aspects. Terminal differentiation of VEC is accompanied by the loss of majority of the organelles including the nucleus. To understand the mechanisms that underlie this process we have analysed the regulation of DNase I (a key effector of apoptotic cell death) in rat VEC under the influence of oestradiol. The present study demonstrates that under physiological conditions, cell death in the VEC is mainly through terminal differentiation although a few cells may undergo apoptotic death involving DNA fragmentation. Unaltered levels of bcl-2 message upon oestradiol administration suggest an important role played by this molecule in preventing death of the VEC by apoptosis. |
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| Keywords: | oestradiol vaginal epithelial cells programmed cell death DNase I in situ hybridization |
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