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Published on: June 29, 2013
OS079. Fetal deglycosylated apolipoprotein C-III (Apo C-III0) concentration is altered in intrauterine growth
1Department of Obstetrics and Gynecology, University Hospital of the RWTH Aachen, Aachen, Germany.
Insights
Researchers identified a unique proteome signature in umbilical cord blood from fetuses with intrauterine growth restriction (IUGR). A specific form of apolipoprotein C-III (apoC-III0) was elevated in IUGR, potentially impairing triglyceride metabolism.
Area of Science:
- Biochemistry
- Proteomics
- Metabolomics
Background:
- Intrauterine growth restriction (IUGR) is associated with altered serum lipid levels.
- Understanding metabolic changes in IUGR fetuses is crucial for diagnosis and management.
Purpose of the Study:
- To analyze the proteome profile of umbilical cord blood in IUGR fetuses.
- To identify specific proteins and metabolic alterations associated with IUGR.
Main Methods:
- Proteomic analysis of umbilical cord blood serum from IUGR and control groups using MALDI-TOF mass spectrometry.
- Protein identification via SDS-PAGE and peptide mass fingerprinting.
- Quantification of specific proteins by ELISA and statistical analysis.
Main Results:
- A distinct proteome signature was identified in IUGR samples, with six key ion signals differentiating groups.
- Elevated levels of deglycosylated apolipoprotein C-III (apoC-III0) were observed in IUGR.
- Increased fetal triglyceride levels in IUGR were significantly correlated with higher apoC-III0 concentrations.
Conclusions:
- A proteome signature from umbilical cord blood can identify IUGR.
- Elevated apoC-III0 in IUGR may reduce triglyceride catabolism, contributing to observed hypertriglyceridemia.
- Altered protein glycosylation is a potential factor in IUGR pathophysiology.
Introduction:
We recently demonstrated that serum lipid levels are altered in growth restricted fetuses (IUGR) [1].
Objectives:
We now aimed to analyse the proteome profile of umbilical cord blood in order to gain a greater understanding about metabolic changes in IUGR fetuses.
Methods:
umbilical cord blood serum samples of IUGR (n=15) and of gestational age matched controls (CN; n=15) were subjected to fractionation by affinity chromatography using a bead system with hydrophobic interaction capabilities. So prepared protein mixtures were forwarded to MALDI-TOF mass spectrometric profiling. Assignment of ion signals in the mass spectra to specific proteins was substantiated by SDS-PAGE in conjunction with peptide mass fingerprint analysis. Concentrations of proteins of interest were additionally measured by ELISA. Statistical estimations were performed by Student's t-test and calculation of Spearman's correlation coefficient.
Results:
MALDI mass spectra showed on average more than 60 protein ion signals between m/z 4000 and 25,000. The six best differentiating ion signals were found at m/z 8205, m/z 8766, m/z 13,945, m/z 15,129, m/z 15,308, and m/z 16,001. One of the constituent of this proteome signature is the deglycosylated form of apolipoprotein C-III, apo C-III0 (8766 m/z) that is known to prevent triglycerides from catabolism. While total Apo CIII concentration tended to be decreased (IUGR 22.54μg/mL SD 10.25. CN 29.9μg/mL SD 15.46. p=0.1355) calculated Apo C-III0 concentration levels has been found to be more abundant in the IUGR cord blood serum samples (IUGR 1.99μg/mL SD 0.85. CN 1.15μg/mL SD 0.55. p<0.0001). Moreover, fetal triglycerid levels were significantly increased in IUGR (IUGR 16.7mg/dL SD 7.58. CN 56.5mg/dL SD 49.92. p-value after log transformation =0.0008)and apo C-III0 was highly correlated to fetal triglyceride levels (rho=0.694).
Conclusion:
Using mass spectrometric approaches we successfully developed an IUGR specific proteome signature derived from human umbilical cord blood samples. Most interesting the deglycosylated form of the apolipoprotein C-III (apoC-III0) was found to be significantly increased in IUGR and thus might lead to reduced triglyceride catabolism. This observation is in agreement with the known observation of triglyceride levels being increased in IUGR fetuses. Our results indicate that subtle alterations in protein glycosylation need to be considered for improving our understanding of the pathomechanisms in IUGR.
