Placental lipase expression in pregnancies complicated by preeclampsia: A case-control study

Barrett, Helen L., Kubala, Marta H., Scholz Romero, Katherin., Denny, Kerina J., Woodruff, Trent M., McIntyre, H.David., Callaway, Leonie K. and Dekker Nitert, Marloes. (2015) Placental lipase expression in pregnancies complicated by preeclampsia: A case-control study. Reproductive Biology and Endocrinology, 13 1: . doi:10.1186/s12958-015-0098-9


Author Barrett, Helen L.
Kubala, Marta H.
Scholz Romero, Katherin.
Denny, Kerina J.
Woodruff, Trent M.
McIntyre, H.David.
Callaway, Leonie K.
Dekker Nitert, Marloes.
Title Placental lipase expression in pregnancies complicated by preeclampsia: A case-control study
Journal name Reproductive Biology and Endocrinology   Check publisher's open access policy
ISSN 1477-7827
Publication date 2015-09-04
Year available 2015
Sub-type Article (original research)
DOI 10.1186/s12958-015-0098-9
Open Access Status DOI
Volume 13
Issue 1
Total pages 9
Place of publication London, United Kingdom
Publisher BioMed Central
Collection year 2016
Language eng
Formatted abstract
Background: Preeclampsia (PE) is associated with maternal and neonatal morbidity and mortality. In PE, the physiological hyperlipidaemia of pregnancy is exaggerated. The purpose of this study was to examine the expression of adipose triglyceride lipase (ATGL), hormone sensitive lipase (HSL), lipoprotein lipase (LPL) and endothelial lipase (EL) in pregnancies complicated by PE.

Methods: Placentae were collected from 16 women with PE and 20 women with uncomplicated pregnancies matched for maternal prepregnancy BMI and gestational age of delivery. Gene and protein expression of the placental lipases were measured by Q-PCR and Western blot. DNA methylation of the promoter of LPL was assessed by bisulfite sequencing. Lipase localisation and activity were analysed.

Results: 
Gene expression of all lipases was significantly reduced, as was HSL protein level in women with PE. All lipases were localised to trophoblasts and endothelial cells in PE and control placentae. There was no difference in methylation of the LPL promoter between PE and control placentae. Lipase activity was not altered in placentae from women with PE.

Conclusion: These results suggest that the decreased placental lipase gene but not protein expression or lipase activity, which is associated with late-onset PE is not a major contributor to the abnormal lipids seen in PE.
Keyword Preeclampsia
Intrauterine growth restriction
Lipase
Placenta
Pregnancy
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

 
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