OBJECTIVE: Our objective was to determine signaling molecules and apoptosis rate in the term placenta of a baboon model of maternal nutrient reduction (MNR). STUDY DESIGN: Female baboons were fed ad libitum for controls (n = 7) or 70% of control baboon diet (MNR; n = 6) from 30-165 days of gestation with necropsy at 165 days of gestation. Placental tissues were collected and fixed for immunohistochemistry or snap frozen to measure extracellular signal-regulated kinases, protein kinase B, JUN NH(2)-terminal kinase, X-linked inhibitor of apoptosis protein, and caspase 3. Placental villous apoptosis was determined by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling and cytokeratin 18 cleavage. RESULTS: Compared with the control placentas, MNR placentas demonstrated reduced placental weight (P < .02), decreased phospho (p)-ERK (P < .04), increased placental villous apoptosis (P < .001), increased villous cytokeratin 18 cleavage, increased X-linked inhibitor of apoptosis protein (P < .007), and increased active caspase 3 (P < .02). CONCLUSION: We conclude that placental apoptosis is increased in this baboon model of MNR at term and that the increase in X-linked inhibitor of apoptosis protein may be a protective mechanism against this apoptosis. Published by Mosby, Inc.
OBJECTIVE: Our objective was to determine signaling molecules and apoptosis rate in the term placenta of a baboon model of maternal nutrient reduction (MNR). STUDY DESIGN: Female baboons were fed ad libitum for controls (n = 7) or 70% of control baboon diet (MNR; n = 6) from 30-165 days of gestation with necropsy at 165 days of gestation. Placental tissues were collected and fixed for immunohistochemistry or snap frozen to measure extracellular signal-regulated kinases, protein kinase B, JUN NH(2)-terminal kinase, X-linked inhibitor of apoptosis protein, and caspase 3. Placental villous apoptosis was determined by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling and cytokeratin 18 cleavage. RESULTS: Compared with the control placentas, MNR placentas demonstrated reduced placental weight (P < .02), decreased phospho (p)-ERK (P < .04), increased placental villous apoptosis (P < .001), increased villous cytokeratin 18 cleavage, increased X-linked inhibitor of apoptosis protein (P < .007), and increased active caspase 3 (P < .02). CONCLUSION: We conclude that placental apoptosis is increased in this baboon model of MNR at term and that the increase in X-linked inhibitor of apoptosis protein may be a protective mechanism against this apoptosis. Published by Mosby, Inc.
Authors: V S Ratts; X J Tao; C B Webster; P E Swanson; S D Smith; P Brownbill; S Krajewski; J C Reed; J L Tilly; D M Nelson Journal: Placenta Date: 2000-05 Impact factor: 3.481
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