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Publications

Placental expression of miR-517-5p and miR-518f-5p: Fetal sex-specific relations with human fetoplacental growth.

Groups and Associations Prachi Kochhar, Pratibha Dwarkanath, Gayatri Ravikumar, Annamma Thomas, Julian Crasta, Tinku Thomas d, Anura V. Kurpad a, Arpita Mukhopadhyay
European Journal of Obstetrics and Gynecology and Reproductive Biology 2022

Abstract

Objective

We aimed to assess association of chromosome 19 miRNA cluster microRNAs (miR-517-5p and miR-518f-5p) expression with maternal, placental and newborn parameters and with their potential angiogenesis-associated target genes ENG, VEGF and FLT in a set of 68 small- (SGA, n = 30) and appropriate- (AGA, n = 38) for gestational age full-term singleton pregnancies, in relation to fetal sex.

Study design

In this retrospective case-control study, placental transcript abundances of miR-517-5p and miR-518f-5p were assessed by real-time quantitative PCR after normalization to reference miRNA, mir-16-5p. Placental transcript abundances of VEGF, FLT and ENG were assessed after normalizing to a set of reference genes.

Results

Placental miR-517-5p transcript abundance was negatively associated with birth weight [β = −88.778, P = 0.006, 95% confidence interval (CI): −151.645, −25.911] and placental weight (β = −14.683, P = 0.007, 95% CI: −25.254, −4.112) and this association with birth weight was specific to the AGA births (β = −59.207, P = 0.037, 95% CI: −114.522, −3.891). miR-518f-5p transcript abundance was negatively associated with placental weight (β = −6.250, P = 0.034, 95% CI: −11.940, −0.559) specifically in the AGA male births (n = 16). Placental VEGF transcript abundance was negatively associated with that of miR-517-5p specifically in SGA female births (n = 14; Spearman's ρ = −0.705, P = 0.005) and with miR-518f-5p transcript abundance specifically in SGA births (Spearman's ρ = −0.437, P = 0.016) and in SGA male births (n = 16; Spearman's ρ = −0.516, P = 0.041).

Conclusion

We conclude that placental miR-517-5p could be playing a key role in the pathophysiology of fetal growth restriction, which can be potentially targeted through maternal lifestyle modifications for improving fetoplacental growth.