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Cytosolic phospholipase A₂ is crucial for ‘on-time’ embryo implantation that directs subsequent development

¹ Departments of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160-7336, USA
² Departments of Obstetrics and Gynecology, Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110, USA
³ Department of Pediatrics, University of Kansas Medical Center, Kansas City, KS 66160-7336, USA
⁴ Department of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232-2279, USA
⁵ Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA

*Author for correspondence (e-mail: sdey{at}kumc.edu)

Accepted 26 March 2002

Cytosolic phospholipase A₂ (cPLA₂) is a major provider of arachidonic acid (AA) for the cyclooxygenase (COX) system for the biosynthesis of prostaglandins (PGs). Female mice with the null mutation for Pla2g4a (cPLA₂) produce small litters and often exhibit pregnancy failures, although the cause(s) of these defects remains elusive. We show that the initiation of implantation is temporarily deferred in Pla2g4a^–/– mice, shifting the normal ‘window’ of implantation and leading to retarded feto-placental development without apparent defects in decidual growth. Furthermore, cPLA₂ deficiency results in aberrant uterine spacing of embryos. The deferred implantation and deranged gestational development in Pla2g4a^–/– mice were significantly improved by exogenous PG administration. The results provide evidence that cPLA₂-derived AA is important for PG synthesis required for on-time implantation. This study in Pla2g4a^–/– mice, together with the results of differential blastocyst transfers in wild-type mice provides the first evidence for a novel concept that a short delay in the initial attachment reaction creates a ripple effect propagating developmental anomalies during the subsequent course of pregnancy.

Key words: cPLA₂, implantation, uterus, embryo, pregnancy

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