OESTRADIOL REGULATED PROGRAMMED CELL DEATH IN RAT VAGINA: TERMINAL DIFFERENTIATION OR APOPTOSIS?
Version of Record online: 2 JAN 2013
© The Author(s) Journal compilation © 1998 International Federation for Cell Biology
Cell Biology International
Volume 22, Issue 2, pages 105–113, February 1998
How to Cite
RAO, K. S., ZANOTTI, S., REDDY, A. G., RAUCH, F., MANNHERZ, H. G. and GUPTA, P. D. (1998), OESTRADIOL REGULATED PROGRAMMED CELL DEATH IN RAT VAGINA: TERMINAL DIFFERENTIATION OR APOPTOSIS?. Cell Biology International, 22: 105–113. doi: 10.1006/cbir.1998.0230
- Issue online: 2 JAN 2013
- Version of Record online: 2 JAN 2013
- Accepted 28 January 1998 Received 25 September 1997
- Cited By
- vaginal epithelial cells;
- programmed cell death;
- DNase I;
- in situ hybridization
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.