title: Steady-state luteinizing hormone receptor messenger ribonucleic acid levels and endothelial cell composition in bovine normal- and short-lived corpora lutea.
abstract: The short-lived corpus luteum (CL) contributes to reproductive inefficiency during the postpartum period in beef cows. The cause for the early demise of the short-lived CL is not fully understood but is believed to involve a premature release of prostaglandin F2 alpha. The objectives of this study were to evaluate norgestomet-hCG-induced normal-lived CL and hCG-induced short-lived CL in postpartum cows with respect to serum progesterone (P4) and 13,14-dihydro-15-keto, prostaglandin F2 alpha (PGFM) concentrations and luteal LH receptor (LH-R) concentrations, LH-R mRNA levels, and vascularity. Although serum P4 profiles from the time of hCG administration (Day 0) until luteectomy (Day 6, 7, or 8) were similar between CL life span groups, PGFM concentrations were elevated (p < 0.05) on Day 8 in cows expected to have short-lived CL compared to normal-lived CL. The LH-R concentrations were similar between normal- and short-lived CL on all days measured. Irrespective of luteal life span and day of luteectomy, all CL possessed a 4.4-kb LH-R transcript. Actin-normalized LH-R mRNA levels were similar between normal- and short-lived CL on Days 6 and 7; however, Day 8 short-lived CL contained less (p < 0.05) LH-R mRNA than Day 8 normal-lived CL. Although the area of luteal tissue occupied by capillaries in normal- and short-lived CL was similar on Days 6 and 7, the area occupied by capillaries in short-lived CL was lower (p < 0.05) than that for normal-lived CL on Day 8. Collectively, these results indicate that there is a decrease in steady-state LH-R mRNA and a reduction in luteal vascularity in CL expected to be short-lived. These changes occur concomitantly with a rise in serum PGFM, but prior to a decline in serum P4.
authors.affiliation: Department of Animal Sciences, Washington State University, Pullman 99164, USA.
authors.forename: G D
authors.initials: GD
authors.lastname: Smith
authors.forename: H R
authors.initials: HR
authors.lastname: Sawyer
authors.forename: M A
authors.initials: MA
authors.lastname: Mirando
authors.forename: M D
authors.initials: MD
authors.lastname: Griswold
authors.forename: A
authors.initials: A
authors.lastname: Sadhu
authors.forename: J J
authors.initials: JJ
authors.lastname: Reeves
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D002417:Cattle; D006063:Chorionic Gonadotropin / Q000008:administration & dosage; D003338:Corpus Luteum / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D005260:Female; D011282:Pregnenediones / Q000008:administration & dosage; D011374:Progesterone / Q000097:blood / Q000378:metabolism; D045167:Progesterone Congeners / Q000008:administration & dosage; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D011974:Receptors, LH / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D014018:Tissue Distribution / Q000187:drug effects / Q000502:physiology
chemical_list: D006063:Chorionic Gonadotropin; D011282:Pregnenediones; D045167:Progesterone Congeners; D012333:RNA, Messenger; D011974:Receptors, LH; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; C100284:norgestomet; D011374:Progesterone; D015237:Dinoprost