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78 ABSTRACT #P-H5 A NOVEL ROLE FOR UROCORTIN 2 IN CELL CYCLING REGULATION Letizia Galleri [PD] (1), John .R.G. Challis (1, 2), Isabella Caniggia (1, 3, 4) (1) Department of Physiology, University of Toronto, (2) Michael Smith Foundation for Health Research, Vancouver, BC, (3) Samuel Lunenfeld Research Institute, Mount Sinai Hospital, (4) Department of Obstetrics and Gynecology, University of Toronto. Objective: Pre-eclampsia is a syndrome typical of human pregnancy, characterized by decreased utero-placental perfusion and aberrant cell turnover, including increased apoptosis of trophoblast cell. Presently, the mechanisms regulating trophoblast cell turnover in pre-eclampsia are not fully elucidated. Corticotropin-releasing hormone (CRH) and Urocortin 1 (Ucn) are peptides belonging to the family of stress-hormones, involved in stress-induced responses. Two peptides recently discovered, Urocortin 2 (Ucn2) and Urocortin 3 (Ucn3), belong to the same family. All peptides are expressed in the human placenta and membranes, and are secreted in the biological fluids. They are able to bind CRH receptor type I or type II (CRHRI CRHRII). In the event of stress, maternal or fetal physiologic and pathologic conditions may influence placental secretion of CRH and CRHrelated peptides. While it is well known that placental CRH and maternal and fetal plasma levels of Ucn are increased in pre-eclampsia, little is known about Ucn2 and Ucn3 in this syndrome. Therefore, the aims of this study were: 1) to evaluate Ucn2 and Ucn3 mRNA expression levels in pre-eclamptic placentae, and 2) to examine the effects of Ucns on cell cycle and on cell death. Methods: Human placental samples were collected from pre-eclamptic and age-matched control placentae following informed written consent. Changes in placental mRNA expression of Ucn2 and Ucn3 were evaluated by quantitative RT-PCR. Primary cytotrophoblast cells were cultured for 24 h alone, with vehicle or with increasing Ucn2 concentrations (10 -9 and 10 -7 M). The common markers of cell proliferation as well as apoptosis were measured after stimulation. Intracellular over-expression of Ucn2 vector was assessed by transient transfection of JEG cells and CHO cells - human choriocarcinoma and Chinese Hamster Ovary cell lines, respectively - at 12 and 24 hours, at 3% and 20% of oxygen tension. Effects of Ucn2 treatment, Ucn2 over-expression and its effect on markers of mitogenic activity and markers of apoptosis, were assessed by western blot. Results: Pre-eclamptic placentae showed an increase in Ucn2 and Ucn3 mRNA expression, as compared to age-matched control tissues. Treatment of primary cytotrophoblast cells with synthetic peptide Ucn2 increased PCNA (proliferating cell nuclear antigen) levels at both concentrations. Markers of apoptosis did not exhibit any change when compared to negative controls. Intracellular Ucn2 over-expression did not show any effect on transfected JEG cells and CHO cells, irrespective of time or oxygen tension. Conclusions: Our data suggest that Ucn2 can be involved in the mechanisms regulating trophoblast cell cycle through an extracellular pathway, activating the CRHRII receptor, which is specific to Ucn2. No intracellular pathways are activated by Ucn2 in either transfected cell line. It is possible that enhanced Ucn2 expression in pre-eclampsia may contribute to impaired trophoblast cell turnover typical of this disorder. Intracellular mechanisms by which Ucn2 may carry out this function remain to be elucidated.
79 ABSTRACT #P-I1 VASCULAR DYSFUNCTION IN WOMEN WITH A HISTORY OF PRE-ECLAMPSIA AND INTRAUTERINE GROWTH RESTRICTION: INSIGHTS INTO FUTURE CARDIOVASCULAR RISK Yoav Yinon [F](1), David Cherney(2), Ori Nevo(3), John Kingdom(1), Michelle Hladunewich(2) (1) Maternal-Fetal Medicine Division, Department of Obstetrics and Gynecology, Mount Sinai Hospital, (2) Division of Nephrology, University Health Network, Toronto General Hospital, (3) Department of Obstetrics and Gynecology, Sunnybrook Health Sciences Centre, University of Toronto, Toronto Objective: Women with a history of preeclampsia or intra-uterine growth restriction (IUGR) are at increased risk for the future development of hypertension and cardiovascular disease. The aim of this study was to examine whether vascular function is impaired in postpartum women with a history of preeclampsia or IUGR by measuring endothelial function and arterial stiffness. Methods: Healthy women with a history of early onset pre-eclampsia (n=10), late onset preeclampsia (n=5), IUGR without pre-eclampsia (n=5) and prior normal pregnancy (n=10) were studied 6-24 months after delivery. Endothelial-dependent vasodilatation and endothelialindependent vasodilatation were studied using high-resolution ultrasound by examination of the brachial artery responses to post-ischemic reactive hyperemia and sublingual glycerylnitrate. Carotid and radial arterial stiffness were assessed by pulse-wave analysis. Laboratory evaluation included fasting insulin and glucose levels, a lipid profile and a urine albumin to creatinine ratio. Results: Baseline BMI, mean arterial pressure, and fasting glucose, insulin and cholesterol levels did not significantly differ among the groups. Endothelial-dependent vasodilatation was significantly reduced in women with previous pre-eclampsia or IUGR compared to women with previous normal pregnancy (4.1 % vs 8%, p=0.02), whereas endothelial-independent vasodilatation was similar in both groups (18.6% vs 17.13%, p=0.44). Radial arterial stiffness in the previously pre-eclamptic or IUGR groups was significantly increased with an augmentation index of 26.4% compared to 14.5% in the control group (p=0.001). Sub-group analysis demonstrated impaired endothelial-dependent vasodilatation in women with previous early-onset pre-eclampsia as well as women with previous IUGR without pre-eclampsia compared to the control group (3.3 % vs 8%, p=0.015; 2.6% vs 8%, p= 0.03). In women with a history of late-onset pre-eclampsia, endothelialdependent vasodilatation was not significantly different compared to the control group (6.6% vs 8%, p= 0.55). Conclusions: Women with a history of early onset pre-eclampsia as well as women with previous IUGR without pre-eclampsia exhibit impaired vascular function. This observation might explain the higher risk of cardiovascular disease in these women. Women with a history of late-onset preeclampsia, however, may not fall into this high cardiovascular risk category. Funded by: PSI Foundation
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Department of Obstetrics and Gynaec
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2 PROGRAMME-AT-A-GLANCE (A.M.) 7:30
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5 PROGRAMME 26TH ANNUAL RESEARCH DA
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7 P-A4 PHENOTYPE OF EARLY ONSET INT
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9 P-C2 ESTROGEN EXTRACTION FROM MIC
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11 P-E4 LAPAROSCOPIC PERITONEAL ENT
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13 12:05 - 1:05 p.m. LUNCH [Dining
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15 P-G2 P16 ONCOPROTEIN AS A TRIAGE
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17 GROUP I: Chairs/Judges: Drs. Jon
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19 GROUP K: Chairs/Judges: Drs. Gra
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21 4:15 - 5:15 p.m. Henderson Lectu
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23 AWARDS The Papsin Award The Dr.
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26 ABSTRACT #O1* CO-ENZYME Q10 SUPP
Page 30 and 31: 28 ABSTRACT #O3* VEPH1 IS A NOVEL R
Page 32 and 33: 30 ABSTRACT #O5* TISSUE SPECIFIC TR
Page 34 and 35: 32 ABSTRACT #O7 JOB SATISFACTION AM
Page 36 and 37: 34 ABSTRACT #O9 ABDOMINAL VISCERAL
Page 38 and 39: 36 ABSTRACT #O11 REGULATORY EFFECTS
Page 40 and 41: 38 ABSTRACT #O13 THE EFFECT OF CHRO
Page 42 and 43: POSTER ABSTRACTS 40
Page 44 and 45: 42 ABSTRACT #P-A2 INCREASED MATERNA
Page 46 and 47: 44 ABSTRACT #P-A4 PHENOTYPE OF EARL
Page 48 and 49: 46 ABSTRACT #P-B1* ANGIOGENIC CD56
Page 50 and 51: 48 ABSTRACT #P-B3 UNDERSTANDING THE
Page 52 and 53: 50 ABSTRACT #P-B5 LOW VITAMIN D LEV
Page 54 and 55: 52 ABSTRACT #P-C2* ESTROGEN EXTRACT
Page 56 and 57: 54 ABSTRACT #P-C4 PRETERM PERMATURE
Page 58 and 59: 56 ABSTRACT #P-D2 CRYOPRESERVATION
Page 60 and 61: 58 ABSTRACT #P-D4 DIFFERENTIAL EXPR
Page 62 and 63: 60 ABSTRACT #P-E1 THE ROLE OF ANDRO
Page 64 and 65: 62 ABSTRACT #P-E3 CELL CYCLE INHIBI
Page 66 and 67: 64 ABSTRACT #P-F1 DEXAMETHASONE STI
Page 68 and 69: 66 ABSTRACT #P-F3 EDUCATING SURGICA
Page 70 and 71: 68 ABSTRACT #P-F5 OUTCOMES IN ROBOT
Page 72 and 73: 70 ABSTRACT #P-G2 P16 ONCOPROTEIN A
Page 74 and 75: 72 ABSTRACT #P-G4 ALTERED ADRENOCOR
Page 76 and 77: 74 ABSTRACT #P-H1 RETINAL HEMORRHAG
Page 78 and 79: 76 ABSTRACT #P-H3 A ROLE FOR MCL-1
Page 82 and 83: 80 ABSTRACT #P-I2 THE TIMING OF DEL
Page 84 and 85: 82 ABSTRACT #P-I4 OMEGA-3 FATTY ACI
Page 86 and 87: 84 ABSTRACT #P-J1* WHAT IS KEEPING
Page 88 and 89: 86 ABSTRACT #P-J3 HUMAN EMBRYONIC F
Page 90 and 91: 88 ABSTRACT #P-J5 BARRIERS TO COMPL
Page 92 and 93: 90 ABSTRACT #P-K2 THE “DUC” TRI
Page 94 and 95: 92 ABSTRACT #P-K4 IS THERE A ROLE F
Page 96 and 97: 94 ABSTRACT #P-L1 EXPRESSION AND RE
Page 98 and 99: 96 ABSTRACT #P-L3 IS ZONA PELLUCIDA
Page 100 and 101: 98 ABSTRACT #P-L5 SPECTRUM OF VASCU
Page 102 and 103: 100 Presenters by Last Name cont’
Page 104 and 105: 102 Presenters by Abstract # and Se
Page 106 and 107: 104 Presenters by Abstract # and Se
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