Objective: The aim of the present study was to detect the role of G protein-associated estrogen receptor (GPER) 1, corin, raftlin and estrogen in etiopathogenesis of intrauterine growth retardation (IUGR).Materials and methods: The present study was designed prospectively between January 2017 and May 2018. The study group included 32 patients with unexplained IUGR and 32 healthy pregnant women who gave birth at term among the patients who referred to obstetrics clinic of a tertiary reference hospital. Intrauterine growth retardation (IUGR) was accepted as birth weight below 10th percentile according to the estimated fetal weight. Exclusion criteria were as follows: the patients with renal or hepatic dysfunction, presence of any chronic disease, smoker patients, preeclampsia, acute or chronic inflammatory diseases, body mass index as <18 kg/m² and >25 kg/m², structural or chromosomal abnormality in fetus Estradiol (E2), estriol (E3), GPER, corin, and raftlin levels were analyzed in maternal serum and placental tissue homogenate through ELISA method.Results: Serum levels of GPER-1, raftlin, and E3 were significantly lower in IUGR group when compared with the control group (p < .05 for all). Serum corin and E2 levels were similar between two groups. GPER-1, E2, E3, raftlin, and corin levels in placental homogenate were found significantly higher in the control group (p < .05 for all).Conclusion: Although maternal, fetal, and placental causes take place in etiopathogenesis of IUGR, exact etiological factor is not revealed in majority of the IUGR cases. The present study serves as the first study revealing the role of the decrease in GPER-1 and raftlin in maternal serum and placental levels on the etiopathogenesis of IUGR. Furthermore, the decrease in placental corin expression of the cases with IUGR was detected first in the literature. The present study reveals a potential therapeutic use of GPER-1, corin, and raftlin for IUGR.

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