Neonatal HDL Counteracts Placental Vascular Inflammation via S1P–S1PR1 Axis

Placental inflammation and dysfunction during pregnancy are associated with short- and long-term adverse outcomes for the offspring. However, the mechanisms of vascular protection at the feto-placental interface are still poorly investigated. The high-density lipoprotein (HDL) associated sphingosine...

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Veröffentlicht in:International journal of molecular sciences Jg. 21; H. 3; S. 789
Hauptverfasser: Del Gaudio, Ilaria, Hendrix, Sebastian, Christoffersen, Christina, Wadsack, Christian
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland MDPI AG 25.01.2020
MDPI
Schlagworte:
Apoptosis
Atherosclerosis
Cardiovascular disease
Cholesterol
Communication
Cytokines
Diabetes
Endothelium
Fetuses
Gene expression
Homeostasis
Inflammation
Nitric oxide
Physiology
Preeclampsia
Pregnancy
Reactive oxygen species
vascular inflammation
sphingosine-1-phosphate
neonatal high-density lipoprotein
feto-placental dysfunction
ISSN:1422-0067, 1661-6596, 1422-0067
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Zusammenfassung:Placental inflammation and dysfunction during pregnancy are associated with short- and long-term adverse outcomes for the offspring. However, the mechanisms of vascular protection at the feto-placental interface are still poorly investigated. The high-density lipoprotein (HDL) associated sphingosine-1-phosphate (S1P) has been described as a powerful anti-inflammatory complex. This study aimed to elucidate the role of cord blood-derived HDL (nHDL) in feto-placental endothelial dysfunction. Here, we report that the exposure of primary fetal placental arterial endothelial cell (fPAEC) to healthy nHDL-S1P attenuated the ability of TNFα to activate NF-κB signaling and increase the expression of pro-inflammatory markers. Moreover, the angiotensin II (AngII)-induced reactive oxygen species (ROS) production was blunted in the presence of nHDL, whereas it was preserved when the cells were preincubated with S1P receptor antagonists, suggesting that S1P accounts for the vascular protective function of nHDL at the feto-placental unit. These results highlight the importance of HDL and S1P metabolism and signaling in pregnancy pathophysiology.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21030789