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ELABELA/APELA Levels Are Not Decreased in the Maternal Circulation or Placenta among Women with Preeclampsia.

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Pritchard, Natasha 
Kaitu'u-Lino, Tu'uhevaha J 
Gong, Sungsam 
Dopierala, Justyna 
Smith, Gordon CS 


The genetic deletion of apelin receptor early endogenous ligand (Elabela; official name APELA) produces a preeclampsia-like phenotype in mice. However, evidence linking ELABELA with human disease is lacking. Therefore, we measured placental mRNA and circulating ELABELA in human samples. ELABELA mRNA (measured by RNA sequencing) was unchanged in 82 preeclamptic placentas compared with 82 matched controls (mean difference, 0.53%; 95% CI, -25.9 to 27.0; P = 0.78). We measured circulating ELABELA in 32 women with preterm preeclampsia (delivered at <34 weeks' gestation) and 32 matched controls sampled at the same gestational age. There was no difference in circulating ELABELA concentrations in the preeclamptic cohort compared with controls (median, 28.5 pg/mL; 95% CI, 5.3 to 63.2 versus median, 20.5 pg/mL; 95% CI, 9.2 to 58.0, respectively); the median difference was 8.0 pg/mL (95% CI, -17.7 to 12.1; P = 0.43). In contrast, soluble FLT1 (a protein with an established association with preeclampsia) mRNA was increased in placental tissue (mean difference, 34.9%; 95% CI, 16.6 to 53.1; P = 0.001), and circulating concentrations were 16.8-fold higher among the preeclamptic cohort (P < 0.0001). In conclusion, we were able to recapitulate the association between circulating soluble FLT1 and preeclampsia, but there was no association with ELABELA. The speculated clinical relevance of observations in the murine model linking ELABELA to preeclampsia likely are incorrect.



Adult, Biomarkers, Case-Control Studies, Female, Humans, Peptide Hormones, Placenta, Pre-Eclampsia, Pregnancy, Prospective Studies

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Am J Pathol

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Elsevier BV
Cambridge University Hospitals NHS Foundation Trust (CUH) (RG52380)
Medical Research Council (G1100221)
Biotechnology and Biological Sciences Research Council (BB/R008590/1)
Medical Research Council (G1100221/1)
Some of the work described was supported by the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (Women’s Health theme), and project grants from the Medical Research Council (United Kingdom; G1100221) and the Stillbirth and neonatal death society (Sands). The study was also supported by GE Healthcare (donation of 2 Voluson i ultrasound systems for this study) and by the NIHR Cambridge Clinical Research Facility, where research visits took place.