Prostaglandin F2α and E1 regulation of proliferation in primary cultures of rabbit endometrial cells
- 1 April 1986
- journal article
- research article
- Published by Wiley in Journal of Cellular Physiology
- Vol. 127 (1) , 55-60
- https://doi.org/10.1002/jcp.1041270108
Abstract
The study of growth of endometrial cells is of importance in reproductive biology. Several factors and hormones are thought to play important roles in the control of growth. Prostaglandin F2α (PGF2α) causes an increase in both tritiated thymidine ([3H]Tdr) incorporation into DNA and in the cell number of primary cultures of rabbit endometrial cells cultured in a serum‐free, chemically defined media. Prostaglandins F1α, E1, E2, A2, and B2 and arachidonic acid (all tested at 10−7 M) do not affect [3H]Tdr incorporation as compared to control cultures. The increase in [3H]Tdr incorporation into DNA in response to PGF2α stimulation is concentration‐dependent (optimal ∼3 × 10−7 M) and is seen starting ∼9 hr poststimulation. Both prostaglandin E1 (PGE1) and prostaglandin E2 (PGE2), but not PGs F1α, I2, A2, B2, their parent molecules, or related molecules, antagonize and can completely block the PGF2α‐induced increase in [3H]Tdr incorporation into DNA. This antagonism is seen both when the cells are pretreated with PGE1 prior to the PGF2α stimulation and when the cells are exposed to both PGE1 and PGF2α simultaneously. Exogenously added 8‐Br‐cAMP mimics the PGE1 antagonism of PGF2α. The PGF2α‐induced increase in [3H]Tdr incorporation is not synergistic, antagonistic, or additive with the [3H]Tdr incorporation increase in response to either estradiol‐17β or epidermal growth factor. The specific effect of PGF2α on primary culture endometrial cell growth and its antagonism by PGE1, PGE2, and 8‐Br‐cAMP are new findings.This publication has 21 references indexed in Scilit:
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