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Circulating Stromal Cell-Derived Factor 1α Levels in Heart Failure: A Matter of Proper Sampling
Lesley Baerts1, Yannick Waumans1, Inger Brandt2
1Laboratory of Medical Biochemistry, University of Antwerp, Antwerp, Belgium.
Insights
Stromal cell-derived factor 1α (SDF1α) levels in heart failure patients are higher when collected with a DPP4 inhibitor. This improves biomarker accuracy for cardiac disease research.
Area of Science:
- Biochemistry
- Cardiology
- Biomarker Discovery
Background:
- Stromal cell-derived factor 1α (SDF1α, CXCL12) is a potential biomarker for cardiac diseases.
- Truncated SDF1α forms alter biological activity, complicating interpretation.
- Dipeptidyl peptidase-4 (DPP4) degrades SDF1α.
Purpose of the Study:
- To investigate the impact of DPP4 on SDF1α immunoreactivity.
- To evaluate the effect of DPP4 inhibition during sample collection on measured SDF1α levels.
- To assess SDF1α levels in heart failure patients with varying left ventricular function.
Main Methods:
- Studied SDF1α immunoreactivities with three immunoassays.
- Incubated SDF1α with DPP4 and serum to assess degradation.
- Measured SDF1α and DPP4 activity in heart failure patients using optimized sampling with DPP4 inhibitor.
Main Results:
- DPP4 incubation caused a significant loss of SDF1α immunoreactivity.
- SDF1α levels were significantly higher in heart failure patients with severe left ventricular dysfunction.
- DPP4 activity was decreased in patients with high SDF1α levels, suggesting feedback inhibition.
Conclusions:
- Recommend collecting samples for SDF1α analysis with a DPP4 inhibitor.
- Higher SDF1α levels were observed in specific heart failure subgroups with DPP4 inhibition.
- Further research is needed on the clinical relevance of SDF1α in cardiac disease.
Background:
The chemokine Stromal cell-derived factor 1α (SDF1α, CXCL12) is currently under investigation as a biomarker for various cardiac diseases. The correct interpretation of SDF1α levels is complicated by the occurrence of truncated forms that possess an altered biological activity.
Methodology:
We studied the immunoreactivities of SDF1α forms and evaluated the effect of adding a DPP4 inhibitor in sampling tubes on measured SDF1α levels. Using optimized sampling, we measured DPP4 activity and SDF1α levels in patients with varying degrees of heart failure.
Results:
The immunoreactivities of SDF1α and its degradation products were determined with three immunoassays. A one hour incubation of SDF1α with DPP4 at 37°C resulted in 2/3 loss of immunoreactivity in each of the assays. Incubation with serum gave a similar result. Using appropriate sampling, SDF1α levels were found to be significantly higher in those heart failure patients with a severe loss of left ventricular function. DPP4 activity in serum was not altered in the heart failure population. However, the DPP4 activity was found to be significantly decreased in patients with high SDF1α levels.
Conclusions:
We propose that all samples for SDF1α analysis should be collected in the presence of at least a DPP4 inhibitor. In doing so, we found higher SDF1α levels in subgroups of patients with heart failure. Our work supports the need for further research on the clinical relevance of SDF1α levels in cardiac disease.
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