title: Endocrine and cellular characteristics of corpora lutea from cows with a delayed post-ovulatory progesterone rise.
abstract: The timing of the post-ovulatory progesterone rise is critical to the embryonic development and survival. The aim of this study was to determine the underlying causes of delayed post-ovulatory progesterone rises. Two groups of non-lactating dairy cows with early (n = 11) or late (n = 9) post-ovulatory progesterone rises were created by inducing luteolysis in the presence of either a large (> 10 mm) or small (< 10 mm) follicle, respectively. LH pulses were measured on days 4 (all cows) and 7 (n = 7, early; n = 5, late) (day 1= ovulation). The cows were slaughtered on day 5 (n = 4 each group) or 8 (n = 7, early; n = 5, late). Immunohistochemical analysis for endothelial cells (von Willebrand Factor, VWF), steroidogenic cells (3beta-HSD) and proliferation marker (Ki67) were performed. The basal progesterone production and LH responsiveness (0.001-100 ng/ml) of dispersed luteal cells was investigated. The luteal concentrations of FGF-2 and VEGF were measured by ELISA and RIA, respectively. There were no differences in LH pulse characteristics, area of VWF staining, proliferation index, steroidogenic cell characteristics, basal or LH-stimulated progesterone production by luteal cells between cows with an early or late progesterone rise (P > 0.10). However, the area of VWF staining increased from days 5 to 8, while the proliferation index decreased (P < 0.05). Furthermore, the luteal cells were more responsive to LH on day 8 (P < 0.01). Luteal concentrations of FGF-2 were higher on day 5 (P = 0.05), while VEGF was greater on day 8 (P < 0.01). In conclusion, we have clearly shown that LH support, degree of vascularization or luteal cell steroidogenic capacity were not the major factors responsible for inadequate secretion of progesterone by the developing bovine CL.
authors.affiliation: Division of Animal Physiology, University of Nottingham, Sutton Bonington Campus, Loughborough, Leics LE12 5RD, UK. Bob.Robinson@nottingham.ac.uk
authors.forename: R S
authors.initials: RS
authors.lastname: Robinson
authors.forename: A J
authors.initials: AJ
authors.lastname: Hammond
authors.forename: L T
authors.initials: LT
authors.lastname: Nicklin
authors.forename: D
authors.initials: D
authors.lastname: Schams
authors.forename: G E
authors.initials: GE
authors.lastname: Mann
authors.forename: M G
authors.initials: MG
authors.lastname: Hunter
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western / Q000662:veterinary; D002417:Cattle / Q000502:physiology*; D049109:Cell Proliferation; D003338:Corpus Luteum / Q000098:blood supply / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006913:Hydroxysteroid Dehydrogenases / Q000378:metabolism; D007150:Immunohistochemistry / Q000662:veterinary; D019394:Ki-67 Antigen / Q000378:metabolism; D016014:Linear Models; D008184:Luteal Cells / Q000166:cytology / Q000502:physiology; D007986:Luteinizing Hormone / Q000097:blood; D018919:Neovascularization, Physiologic / Q000502:physiology; D010062:Ovulation Induction / Q000662:veterinary; D011374:Progesterone / Q000097:blood / Q000502:physiology*; D011897:Random Allocation; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000199:Actins; D019394:Ki-67 Antigen; D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; D016222:Fibroblast Growth Factor 2; D011374:Progesterone; D007986:Luteinizing Hormone; D006913:Hydroxysteroid Dehydrogenases