| Abstract: | Regression of the corpus luteum (CL) is characterized by a decay in progesterone
(P4) production (functional luteolysis) and disappearance of luteal tissues
(structural luteolysis). In mares, structural luteolysis is thought to be caused by
apoptosis of luteal cells, but functional luteolysis is poorly understood.
20α-hydroxysteroid dehydrogenase (20α-HSD) catabolizes P4 into its biologically
inactive form, 20α-hydroxyprogesterone (20α-OHP). In mares, aldo-keto reductase (AKR)
1C23, which is a member of the AKR superfamily, has 20α-HSD activity. To clarify whether
AKR1C23 is associated with functional luteolysis in mares, we investigated the expression
of AKR1C23 in the CL in different luteal phases. The luteal P4 concentration
and levels of 3β-hydroxysteroid dehydrogenase (3β-HSD) mRNA were higher in the mid luteal
phase than in the late and regressed luteal phases (P<0.05), but the level of 3β-HSD
protein was higher in the late luteal phase than in the regressed luteal phase
(P<0.05). The luteal 20α-OHP concentration and the level of AKR1C23
mRNA were higher in the late luteal phase than in the early and mid luteal phases
(P<0.05), and the level of AKR1C23 protein was also highest in the late luteal phase.
Taken together, these findings suggest that metabolism of P4 by AKR1C23 is one
of the processes contributing to functional luteolysis in mares. |
