Tsegaselassie Workalemahu1, Daniel A Enquobahrie1,2, Ermias Yohannes1, Sixto E Sanchez3, Bizu Gelaye4, Chunfang Qiu2, Michelle A Williams4. 1. a Department of Epidemiology , School of Public Health, University of Washington , Seattle , WA , USA . 2. b Center for Perinatal Studies, Swedish Medical Center , Seattle , WA , USA . 3. c Peruana De Ciencias Aplicadas , Lima , Peru , and. 4. d Department of Epidemiology , Harvard T.H. Chan School of Public Health , Boston , MA , USA.
Abstract
OBJECTIVE: To investigate the associations of placental telomere length with placental abruption (PA) risk and interactions between placental telomere length and placental mitochondrial DNA (mtDNA) copy number on PA risk. MATERIALS AND METHODS: Relative telomere length and mtDNA copy number in placental samples collected from 105 cases and 73 controls were measured in two batches using qRT-PCR. Mean differences in relative telomere length between PA cases and controls were examined. After creating batch-specific median cutoffs for relative telomere length (84.92 and 102.53) and mtDNA copy number (2.32 and 1.42), interaction between the two variables was examined using stratified logistic regression models. RESULTS: Adjusted mean difference in relative telomere length between PA cases and controls was -0.07 (p > 0.05). Among participants with low mtDNA copy number, participants with short relative telomere length had a 3.07-fold higher odds (95% CI: 1.13-8.38) of PA as compared with participants with long relative telomere length (the reference group). Among participants with high mtDNA copy number, participants with short relative telomere length had a 0.71-fold lower odds (95% CI: 0.28-1.83) of PA as compared with the reference group (interaction p values = 0.03). CONCLUSION: Findings suggest complex relationships between placental telomere length, mtDNA copy number and PA risk which warrant further larger studies.
OBJECTIVE: To investigate the associations of placental telomere length with placental abruption (PA) risk and interactions between placental telomere length and placental mitochondrial DNA (mtDNA) copy number on PA risk. MATERIALS AND METHODS: Relative telomere length and mtDNA copy number in placental samples collected from 105 cases and 73 controls were measured in two batches using qRT-PCR. Mean differences in relative telomere length between PA cases and controls were examined. After creating batch-specific median cutoffs for relative telomere length (84.92 and 102.53) and mtDNA copy number (2.32 and 1.42), interaction between the two variables was examined using stratified logistic regression models. RESULTS: Adjusted mean difference in relative telomere length between PA cases and controls was -0.07 (p > 0.05). Among participants with low mtDNA copy number, participants with short relative telomere length had a 3.07-fold higher odds (95% CI: 1.13-8.38) of PA as compared with participants with long relative telomere length (the reference group). Among participants with high mtDNA copy number, participants with short relative telomere length had a 0.71-fold lower odds (95% CI: 0.28-1.83) of PA as compared with the reference group (interaction p values = 0.03). CONCLUSION: Findings suggest complex relationships between placental telomere length, mtDNA copy number and PA risk which warrant further larger studies.
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