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HELLP Syndrome

Mareike Sandvoß1, Arne Björn Potthast1, Frauke von Versen-Höynck2

  • 11 Department of Paediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School, Hannover, Germany.

Reproductive Sciences (Thousand Oaks, Calif.)
|September 22, 2016
PubMed

Insights

The hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome impacts fatty acid oxidation. SIRT 4 protein levels increase in endothelial cells during hypoxia in HELLP pregnancies, suggesting a role in metabolic dysfunction.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Disorders

Background:

  • Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome is linked to offspring fatty acid oxidation defects.
  • Fatty acid oxidation is impaired in HELLP syndrome pregnancies and human umbilical vein endothelial cells (HUVECs).
  • Sirtuins, NAD+-dependent deacetylases, regulate cellular metabolic status, with SIRT 4 involved in fatty acid oxidation.

Purpose of the Study:

  • To investigate the role of sirtuins (SIRT 1, SIRT 3, and SIRT 4) in HUVECs from HELLP syndrome pregnancies under hypoxic conditions.
  • To determine if hypoxia affects sirtuin expression and NAD+ levels in HELLP-complicated pregnancies.

Main Methods:

  • Studied SIRT 1, SIRT 3, and SIRT 4 protein levels in HUVECs.
  • HUVECs were from pregnancies with HELLP syndrome and uncomplicated pregnancies (n=7 each).
  • Cells were exposed to hypoxia (2% O2) for varying durations (0, 10, 60, 120 minutes).

Main Results:

  • SIRT 4 protein levels were significantly elevated in HUVECs from HELLP pregnancies after 60 and 120 minutes of hypoxia compared to controls.
  • NAD+ levels demonstrated a time-dependent increase during hypoxia in both groups.
  • SIRT 1 and SIRT 3 levels were not detailed in the provided abstract text.

Conclusions:

  • Hypoxia exacerbates alterations in SIRT 4 expression in HUVECs from HELLP syndrome pregnancies.
  • Increased SIRT 4 under hypoxia may contribute to the compromised fatty acid oxidation observed in HELLP syndrome.
  • Further research is warranted to elucidate the precise mechanisms of sirtuin involvement in HELLP pathophysiology.

Keywords:
HELLP syndromeHUVECsSIRT 4fatty acid oxidationhypoxia

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