title: Vascular and immune regulation of corpus luteum development, maintenance, and regression in the cow.
abstract: The bovine corpus luteum (CL) is a unique, transient organ with well-coordinated mechanisms by which its development, maintenance, and regression are effectively controlled. Angiogenic factors, such as vascular endothelial growth factor A and basic fibroblast growth factor, play an essential role in promoting progesterone secretion, cell proliferation, and angiogenesis. These processes are critically regulated, through both angiogenic and immune systems, by the specific immune cells, including macrophages, eosinophils, and neutrophils, that are recruited into the developing CL. The bovine luteolytic cascade appears to be similar to that of general acute inflammation in terms of time-dependent infiltration by immune cells (neutrophils, macrophages, and T lymphocytes) and drastic changes in vascular tonus and blood flow, which are regulated by luteal nitric oxide and the vasoconstrictive factors endothelin-1 and angiotensin II. Over the period of maternal recognition of pregnancy, the maternal immune system should be well controlled to accept the semiallograft fetus. The information on the presence of the developing embryo in the genital tract is suggested to be transmitted to the ovary by both the endocrine system and the circulating immune cells. In the bovine CL, the lymphatic system, but not the blood vascular system, is reconstituted during early pregnancy, and interferon tau from the embryo could trigger this novel phenomenon. Collectively, the angiogenic and vasoactive factors produced by luteal cells and the time-dependently recruited immune cells within the CL and their interactions appear to play critical roles in regulating luteal functions throughout the life span of the CL.
authors.affiliation: Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Shirasuna
authors.forename: A
authors.initials: A
authors.lastname: Nitta
authors.forename: J
authors.initials: J
authors.lastname: Sineenard
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: H
authors.initials: H
authors.lastname: Bollwein
authors.forename: A
authors.initials: A
authors.lastname: Miyamoto
mesh_terms: D042501:Angiogenic Proteins / Q000502:physiology; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D002417:Cattle / Q000502:physiology*; D003338:Corpus Luteum / Q000098:blood supply / Q000254:growth & development / Q000502:physiology*; D019332:Endothelin-1 / Q000502:physiology; D004804:Eosinophils / Q000276:immunology; D005260:Female; D007107:Immune System / Q000166:cytology / Q000502:physiology*; D003341:Luteolysis / Q000502:physiology*; D008264:Macrophages / Q000276:immunology; D018919:Neovascularization, Physiologic / Q000502:physiology*; D009504:Neutrophils / Q000276:immunology*; D009569:Nitric Oxide / Q000502:physiology; D011247:Pregnancy; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
chemical_list: D042501:Angiogenic Proteins; D019332:Endothelin-1; D042461:Vascular Endothelial Growth Factor A; D000804:Angiotensin II; D009569:Nitric Oxide