Date of Award
Doctor of Philosophy (PhD)
Mammalian corpora lutea (CL) are transient ovarian glands which function to support pregnancy by secretion of progesterone (P). Sustained P secretion during pregnancy in the hamster requires gonadotrophic support, i.e., follicle stimulating hormone (FSH) and prolactin (Prl). Infertile cycles require CL regression. In luteolysis, CL first regress functionally (FL) and then structurally (SL). FL permits the next estrous. Estrous occurs every fourth day in the hamster such that CL form, function briefly, and then regress rapidly and completely. With only one generation of CL present in each ovary at any one time, the hamster is an ideal model for studying luteolysis. FL, begins on day three as P secretion plummets, and is followed immediately by SL as neutrophils —cellular markers of inflammation— invade the CL. SL proceeds via apoptosis and is not reversible with exogenous FSH-Prl.
Apoptosis is synonymous with physiological cell death, and, as a rule, evokes no inflammation. In fact, it may have evolved to prevent inflammation and the excessive tissue damage which often accompanies pathologic cell death. Since apoptosis and inflammation coexist in luteolysis, experiments are designed in the present study to help explain this paradox.
Light and transmission electron microscopic observations of ovarian sections chronicled cyclic luteal morphology. Enzyme histochemistry was conducted on ovarian sections for lysosomal nonspecific esterase activity. Luteal and nonluteal ovarian samples were probed for neutrophilic myeloperoxidase by immunoblot.
Microscopic observations revealed that some luteal cell organelles atrophy in FL prior to the apoptosis seen in SL. Nonspecific esterase staining showed a dramatic increase in autolytic lysosomal activity during SL and follicular atresia. Immunoblots showed that myeloperoxidase is present at the onset of SL.
The findings indicate that luteolysis is a dynamic process which may require a tightly regulated acute inflammatory response for rapid completion. Neutrophils may play a role in the abrupt onset of cell death required for SL. It is possible that in hamster luteolysis the damaging sequalae of chronic inflammation is prevented by apoptosis in which viable luteal cells are transformed into phagocytes that clear the gland of apoptotic cellular debris.
Rodacker, Mark W., "Spontaneous Luteolysis in the Cyclic Golden Hamster: Evidence for Mediation Through Inflammation and Apoptosis" (1995). Theses and Dissertations. 2720.