Placental autotaxin expression is diminished in women with pre-eclampsia

Aim Lysophosphatidic acid (LPA) is a member of a new class of lipid mediators and exerts varied physiological and pathological functions. The secreted protein, autotaxin (ATX), is a key enzymatic determinant of local LPA production. The primary aim of this study was to investigate the potential invo...

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Published inThe journal of obstetrics and gynaecology research Vol. 41; no. 9; pp. 1406 - 1411
Main Authors Ichikawa, Mayuko, Nagamatsu, Takeshi, Schust, Danny J., Kawai-Iwasawa, Yuki, Kawana, Kei, Yamashita, Takahiro, Osuga, Yutaka, Aoki, Junken, Yatomi, Yutaka, Fujii, Tomoyuki
Format Journal Article
LanguageEnglish
Published Australia Blackwell Publishing Ltd 01.09.2015
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Summary:Aim Lysophosphatidic acid (LPA) is a member of a new class of lipid mediators and exerts varied physiological and pathological functions. The secreted protein, autotaxin (ATX), is a key enzymatic determinant of local LPA production. The primary aim of this study was to investigate the potential involvement of the placental ATX–LPA system in pre‐eclampsia (PE). Material and Methods We compared human placental ATX mRNA expression in pregnancies complicated by severe PE with that in healthy placentas using real‐time polymerase chain reaction. We further assessed whether these expression levels were associated with disease‐onset patterns. Results Placental transcription of ATX increased progressively during normal pregnancy. In the analysis for pre‐eclamptic placentas, the placental ATX expression in the early‐onset group, but not in late‐onset group, was significantly lower compared to normal controls. Multiple regression analysis revealed that occurrence of early‐onset PE, but not late‐onset PE, was a variable that was significantly associated with the placental ATX expression level. Conclusion These findings support our previous work showing reduced ATX antigen levels in the peripheral blood of pre‐eclamptic women. A disturbance in placental ATX production may be linked to poor placental development and systemic maternal symptoms in early‐onset PE.
Bibliography:ark:/67375/WNG-BJB314DD-F
istex:7DA6DCD5C7FEFAF7EB5DFE69AAA71394FC9FD0FB
ArticleID:JOG12742
JSPS KAKENHI - No. 23592394, 22890045 and 25861476
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1341-8076
1447-0756
DOI:10.1111/jog.12742