title: Microvascularization and angiogenic activity of equine corpora lutea throughout the estrous cycle.
abstract: Corpus luteum growth and endocrine function are closely dependent on the formation of new capillaries. The objectives of this study were to evaluate (i) tissue growth and microvascular development in the equine cyclic luteal structures; (ii) in vitro angiogenic activity of luteal tissues in response to luteotrophic (LH, PGE(2)) and luteolytic (PGF(2alpha)) hormones and (iii) to relate data to luteal endocrinological function. Our results show that microvascular density was increased in the early and mid luteal phase, followed by a fall in the late luteal phase and a further decrease in the corpus albicans. Hyperplasia of luteal tissue increased until the mid luteal phase and it was followed by tissue regression. Luteal explants were cultured with no hormone added, or with PGF(2alpha), LH, PGE(2), LH+PGE(2) or LH+PGF(2alpha). Media conditioned by equine luteal tissue from different stages of the luteal phase were able to stimulate mitogenesis of bovine aortic endothelial cells (BAEC), suggesting the presence of angiogenic activity. No difference was observed among luteal structures on their mitogenic capacity, for any treatment used. Nevertheless, Late-CL conditioned-media with PGF(2alpha) showed a significant decrease in BAEC proliferation (p<0.05) and LH+PGF(2alpha) a tendency to reduce mitogenesis. Thus, prostaglandin F(2alpha) may play a role on vascular regression of the CL during the late luteal phase in the mare. These data suggest that luteal angiogenesis and vascular regression in the mare are coordinated with the development of non-vascular tissue and might be regulated by many different factors.
authors.affiliation: CIISA, Faculdade de Medicina Veterinária, R. Prof. Cid dos Santos, 1300-477 Lisboa, Portugal. gmlfdias@fmv.utl.pt
authors.forename: G
authors.initials: G
authors.lastname: Ferreira-Dias
authors.forename: P Pinto
authors.initials: PP
authors.lastname: Bravo
authors.forename: L
authors.initials: L
authors.lastname: Mateus
authors.forename: D A
authors.initials: DA
authors.lastname: Redmer
authors.forename: J A
authors.initials: JA
authors.lastname: Medeiros
mesh_terms: D000818:Animals; D002455:Cell Division / Q000187:drug effects; D003338:Corpus Luteum / Q000098:blood supply* / Q000737:chemistry; D017077:Culture Media, Conditioned; D004247:DNA / Q000032:analysis; D015237:Dinoprost / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology; D042783:Endothelial Cells / Q000166:cytology; D030762:Estrous Cycle / Q000502:physiology*; D005260:Female; D006736:Horses / Q000502:physiology*; D007986:Luteinizing Hormone / Q000494:pharmacology; D008833:Microcirculation / Q000166:cytology / Q000502:physiology*; D008938:Mitosis; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000502:physiology*; D011374:Progesterone / Q000032:analysis / Q000097:blood; D011506:Proteins / Q000032:analysis; D012313:RNA / Q000032:analysis; D046509:Tissue Culture Techniques / Q000662:veterinary; D042461:Vascular Endothelial Growth Factor A / Q000494:pharmacology
chemical_list: D017077:Culture Media, Conditioned; D011506:Proteins; D042461:Vascular Endothelial Growth Factor A; D011374:Progesterone; D012313:RNA; D007986:Luteinizing Hormone; D004247:DNA; D015237:Dinoprost; D015232:Dinoprostone