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09:02
Percutaneous Hepatic Perfusion PHP with Melphalan as a Treatment for Unresectable Metastases Confined to the Liver
Published on: July 31, 2016
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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
Summary
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.
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