title: Microvascular endothelial cells of the bovine corpus luteum: a comparative examination of the estrous cycle and pregnancy.
abstract: Endothelial cells derived from the corpus luteum (CLENDOs) exhibit diverse characteristics presumably serving their wide-ranging roles in luteal function and fate. Here, several attributes of CLENDOs derived from cows at midcycle (days 9-12 of the estrous cycle) were compared with CLENDOs from early pregnancy (day 60 of pregnancy). Flow cytometric analysis of cells fluorescently-tagged with the lectins Bandeiraea simplicifolia (BS-1) and Concanavalin A (ConA) indicated that CLENDOs of midcycle CL do not differ from those of pregnancy. Mean fluorescence intensity for BS-1 was 15 +/- 1 and 23 +/- 7 fluorescent units for midcycle CLENDOs and CLENDOs of pregnancy, respectively (P>0.05). For ConA, mean fluorescence was 25 +/- 2 and 26 +/- 1 fluorescent units, respectively (P>0.05). The CLENDOs were also exposed to cytokines to assess differences in activation of nuclear factor kappa B signaling (NF-kappaB), induction of the transcription factor interferon regulatory factor 1 (IRF1), cytokine production, and cytokine-induced cell death. In response to TNF, for instance, both types of CLENDOs exhibited a rapid, 5-fold decrease in NF-kappaB inhibitor alpha (NFKBIA) protein expression (P<0.05), and a 4-fold increase in IRF1 expression (P<0.05), that did not differ with phenotype (P>0.05). Similarly, both types of CLENDOs produced tumor necrosis factor alpha and chemokine ligand 2 in response to IFNG stimulation (P<0.05) that did not differ with phenotype (P>0.05). Lastly, extended exposure of CLENDOs of midcycle CL to cytokines induced cell death (~50% cell death vs. control) similar to the incidence of cell death seen previously in CLENDOs of early pregnancy. The results indicate that several physical and functional characteristics of CLENDOs of midcycle CL are retained through early pregnancy, including lectin-binding properties, sensitivity to cytokines, and the activation of cytokine-initiated intracellular signals.
authors.affiliation: Department of Animal and Nutritional Sciences, University of New Hampshire, Durham, NH 03824, USA.
authors.forename: Jessica Ann
authors.initials: JA
authors.lastname: Cherry
authors.forename: Xiaoying
authors.initials: X
authors.lastname: Hou
authors.forename: Bo Ruben
authors.initials: BR
authors.lastname: Rueda
authors.forename: John Stewart
authors.initials: JS
authors.lastname: Davis
authors.forename: David Harrison
authors.initials: DH
authors.lastname: Townson
mesh_terms: D000818:Animals; D002417:Cattle; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D003208:Concanavalin A; D003338:Corpus Luteum / Q000098:blood supply* / Q000502:physiology; D004268:DNA-Binding Proteins / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D030762:Estrous Cycle / Q000502:physiology*; D005260:Female; D050856:Interferon Regulatory Factor-1 / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism / Q000633:toxicity; D018919:Neovascularization, Physiologic / Q000502:physiology*; D037121:Plant Lectins; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000633:toxicity
chemical_list: D018932:Chemokine CCL2; D004268:DNA-Binding Proteins; C045475:Griffonia simplicifolia lectins; D050856:Interferon Regulatory Factor-1; D037121:Plant Lectins; D014409:Tumor Necrosis Factor-alpha; D003208:Concanavalin A; D007371:Interferon-gamma