title: Luteal activity of pregnant rats with hypo-and hyperthyroidism.
abstract: BACKGROUND
  Luteal activity is dependent on the interaction of various growth factors, cytokines and hormones, including the thyroid hormones, being that hypo- and hyperthyroidism alter the gestational period and are also a cause of miscarriage and stillbirth. Because of that, we evaluated the proliferation, apoptosis and expression of angiogenic factors and COX-2 in the corpus luteum of hypo- and hyperthyroid pregnant rats.
  
  
  METHODS
  Seventy-two adult female rats were equally distributed into three groups: hypothyroid, hyperthyroid and control. Hypo- and hyperthyroidism were induced by the daily administration of propylthiouracil and L-thyroxine, respectively. The administration began five days before becoming pregnant and the animals were sacrificed at days 10, 14, and 19 of gestation. We performed an immunohistochemical analysis to evaluate the expression of CDC-47, VEGF, Flk-1 (VEGF receptor) and COX-2. Apoptosis was evaluated by the TUNEL assay. We assessed the gene expression of VEGF, Flk-1, caspase 3, COX-2 and PGF2α receptor using real time RT-PCR. The data were analyzed by SNK test.
  
  
  RESULTS
  Hypothyroidism reduced COX-2 expression on day 10 and 19 (P < 0.05), endothelial/pericyte and luteal cell proliferation on day 10 and 14 (p < 0.05), apoptotic cell numbers on day 19 (p < 0.05) and the expression of Flk-1 and VEGF on day 14 and 19, respectively (p < 0.05). Hyperthyroidism increased the expression of COX-2 on day 19 (P < 0.05) and the proliferative activity of endothelial/pericytes cells on day 14 (p <0.05), as well as the expression of VEGF and Flk-1 on day 19 (P < 0.05).
  
  
  CONCLUSIONS
  Hypothyroidism reduces the proliferation, apoptosis and expression of angiogenic factors and COX-2in the corpus luteum of pregnant rats, contrary to what is observed in hyperthyroid animals, being this effect dependent of the gestational period.
authors.forename: Juneo Freitas
authors.initials: JF
authors.lastname: Silva
authors.forename: Natália Melo
authors.initials: NM
authors.lastname: Ocarino
authors.forename: Rogéria
authors.initials: R
authors.lastname: Serakides
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000378:metabolism; D003338:Corpus Luteum / Q000378:metabolism*; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D006728:Hormones / Q000097:blood / Q000378:metabolism; D006980:Hyperthyroidism / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D007037:Hypothyroidism / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D064168:Minichromosome Maintenance Complex Component 7 / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D011982:Receptors, Prostaglandin / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000235:genetics / Q000378:metabolism
chemical_list: D006728:Hormones; D011982:Receptors, Prostaglandin; D042461:Vascular Endothelial Growth Factor A; C034671:prostaglandin F2alpha receptor; D051546:Cyclooxygenase 2; D040301:Vascular Endothelial Growth Factor Receptor-2; D053148:Caspase 3; D064168:Minichromosome Maintenance Complex Component 7