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Placental expression of lysophosphatidic acid receptors in normal pregnancy and preeclampsia
Author(s) -
Fujii Tatsuya,
Nagamatsu Takeshi,
Schust Danny J.,
Ichikawa Mayuko,
Kumasawa Keiichi,
Yabe Shinichiro,
Iriyama Takayuki,
Hirota Yasushi,
Osuga Yutaka,
Aoki Junken,
Yatomi Yutaka,
Fujii Tomoyuki
Publication year - 2019
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.13176
Subject(s) - lysophosphatidic acid , preeclampsia , placenta , pregnancy , pathogenesis , immunohistochemistry , receptor , medicine , andrology , fetus , obstetrics , biology , endocrinology , genetics
Problem Recent advances in lipid research have revealed that impairments in lipid mediator signaling can be involved in the pathoetiology of a variety of diseases. We previously reported aberrant expression of autotaxin, a key enzyme for lysophosphatidic acid (LPA) production, in placentas from women with preeclampsia. The present study aimed to further explore the involvement of LPA signaling in the pathoetiology of preeclampsia. Method of study Term placentas were obtained from deliveries after uncomplicated pregnancy (n = 18) and those complicated by preeclampsia (n = 24). First‐trimester placental tissues were collected after elective terminations of pregnancy (n = 20). Placental expression of the six identified LPARs (LPAR1‐6) was analyzed at protein and mRNA levels. Results In normal pregnancy, the mRNA expression levels of all LPARs except LPAR4 were significantly higher in term. Levels of mRNA encoding LPAR2‐5 were significantly increased in preeclampsia placentas compared with those in the normal term placentas. Using Western immunoblotting, only LPAR3 was noted to be increased at the protein level in placentas from preeclamptic pregnancies. This was validated by immunohistochemistry. Conclusion In summary, the placental expression of LPARs, particularly LPAR3, is enhanced in preeclampsia, suggesting that disturbances in placental LPA signaling may be involved in the pathogenesis of preeclampsia.