Yao-Lung Chang, M.D., Chao-Nin Wang, M.D., Ph.D., Pei-Cih Wei, An-Shine Chao, M.D., Shuenn-Dyh Chang, M.D., Po-Jen Cheng, M.D., Tzu-Hao Wang, M.D., Ph.D.
Volume 100, Issue 1, Pages 241-246.e2, July 2013
To study the regulatory mechanisms of selective intrauterine growth restriction (sIUGR) independent of confounding genetic factors, monochorionic (MC) twins are the ideal model, because they have identical genomic DNA. We hypothesize that the intrauterine growth restriction fetus has mitochondrial activation compared with its larger counterpart, and sought to demonstrate this using the MC twin model.
Fetal cord blood and amniotic fluid of MC twins were prospectively collected during delivery. Mitochondrial DNA of cord blood was measured using real-time quantitative polymerase chain reaction (PCR), and mitochondria in amniotic fluid mesenchymal stem cells (AFMSCs) were analyzed with MitoTracker staining.
Tertiary referring center.
Forty-three pairs of MC twins, including 24 pairs with sIUGR and 19 pairs without.
Main Outcome Measure(s):
Mitochondrial DNA contents were measured and presented as fold difference between the small and large fetuses. After staining with MitoTracker, mitochondrial intensity in AFMSCs was analyzed with the Image J program.
The fold differences of the cord blood mitochondrial DNA content between the small and large twins were significantly higher in the MC twins with sIGUR (2.5 ± 1.2, n = 24 pairs) than in those without sIUGR (1.2 ± 0.3, n = 19 pairs). In addition, mitochondrial staining intensities were significantly higher in the AFMSCs derived from growth-restricted fetuses than from control fetuses.
Mitochondrial activation in the sIUGR fetus of MC twins was likely regulated by locally adverse placental and blood flow conditions, instead of genetic factors.
Read the full text at: http://www.fertstert.org/article/S0015-0282(13)00404-4/fulltext