Expression of leptin and leptin receptors in gestational trophoblastic diseases

Abstract

To investigate the expression profile of leptin and leptin receptors in gestational trophoblastic diseases (GTDs). Using immunohistochemical staining on archival paraffin-embedded tissue sections, we studied the expression of leptin and leptin receptor in hydatidiform moles, with gestational age-matched normal first-trimester placenta used as control. A total of 38 cases of hydatidiform moles were studied, including 20 complete moles (CHMs) and 18 partial moles (PHMs). Among them, 10 cases of the CHM group and 8 cases of the PHM group subsequently developed residual trophoblastic disease (RTD). In addition, two cases of choriocarcinoma and three cases of placental site trophoblastic tumor (PSTT) were also studied. Reverse transcriptase-polymerase chain reaction (RT-PCR) was further performed using RNA extracted from frozen tissue (five CHMs, four PHMs and nine normal first-trimester placenta) to study the expression of leptin and individual leptin receptor isoforms at the transcription level. In all tissue sections, immunostaining signal was shown in the cytoplasmic compartment of cytotrophoblasts and syncytiotrophoblasts, with much stronger staining in the former. Significantly higher immunostaining intensity was shown for both leptin (P < 0.05) and leptin receptor (P < 0.001) in both CHMs and PHMs compared to normal first-trimester placenta. There was no significant difference between those cases subsequently developing RTD and those which did not (P > 0.05). In the choriocarcinoma and PSTT cases, intense immunostaining was found in the tumor cells. RT-PCR revealed that the expression of leptin and all leptin receptor isoforms were significantly higher in both CHMs and PHMs than in normal placenta (P < 0.05). There is up-regulated expression of leptin and leptin receptor in GTDs. However, there is no obvious correlation with the development of RTD. The exact role played by leptin and its receptors in the pathogenesis of GTDs awaits further investigations. © 2004 Elsevier Inc. All rights reserved.