PF.07 Expression of 2, 3-Bisphosphoglycerate Mutase (BPGM) in Human Placenta. (26th April 2013)

• Record Type: Journal Article
• Authors: Walter, MNM; Chan, SY; Vatish, M; Kilby, MD
• Is Part Of: Archives of disease in childhood. Volume 98(2013)Supplement 1
• Page Start: A6
• Page End: A6
• Publication Date: 2013-04-26
• Subjects: Infants -- Diseases -- Periodicals; Newborn infants -- Diseases -- Periodicals; Fetus -- Diseases -- Periodicals; 618.920105
• DOI: 10.1136/archdischild-2013-303966.019
• Languages: English
• ISSNs: 1359-2998

Abstract

Abstract : Introduction: BPGM is an enzyme in erythrocytes and trophoblasts, which synthesises 2, 3-bisphosphoglycerate (2, 3-BPG), a facilitator of oxygen liberation from haemoglobin. In an insulin-like growth factor II knockout mouse model of intrauterine growth restriction (IUGR), placental BPGM expression is lower than in wild type animals, implicating BPGM in the pathophysiology of IUGR and suggesting a role for 2, 3-BPG in oxygen delivery to the fetus. Methods: Human placental messenger RNA encoding BPGM was quantified by TaqMan RT-PCR. The relative expression of BPGM was assessed a) over the course of pregnancy at 7–11, 12–20, 24–34 weeks of gestation (w) and term (total n = 68), b) in IUGR placenta at early (24–34 w, n = 15) and late (37–39 w, n = 5) gestations and compared with appropriately grown for gestation age (AGA) controls (n = 8 early, n = 26 late). Results: BPGM mRNA expression significantly increased with advancing gestation (ANOVA p < 0.001). There was a 6 and 7-fold increase from 7–11 w to 24–34 w and term respectively, and 3-fold between 12–20 w and term (p < 0.05 for all). There were no statistically significant differences in BPGM mRNA expression between IUGR and AGA placenta in either gestational age group. Discussion: Levels of BPGM increased in a time-dependant manner to term. This may indicate a protective mechanism to avoid oxidative stress damage during the early stages of fetal development, with BPGM expression increasing over time in response to greater oxygen demand from the growing fetus. Placental BPGM expression does not appear to be implicated in the pathogenesis of IUGR in human.