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CRP Stimulates GDF15 Expression in Endothelial Cells through p53
Yoonseo Kim1, Nicole Noren Hooten1, Michele K Evans1
1Laboratory of Epidemiology and Population Science, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Mediators of Inflammation
|July 4, 2018
Summary
C-reactive protein (CRP) increases Growth Differentiation Factor 15 (GDF15) expression in human aortic endothelial cells. This study reveals a novel link between CRP and GDF15, impacting endothelial inflammation and cardiovascular disease (CVD) pathogenesis.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Inflammation Research
Background:
- Growth differentiation factor 15 (GDF15) is a secreted protein and a potential biomarker for cardiovascular disease (CVD).
- C-reactive protein (CRP) is also an independent biomarker for CVD, associated with inflammation.
- The molecular relationship between GDF15 and CRP has not been previously investigated.
Purpose of the Study:
- To explore the molecular interactions between CRP and GDF15.
- To investigate the effect of CRP on GDF15 expression and its underlying transcriptional mechanisms.
Main Methods:
- Analysis of serum and mRNA levels of hsCRP and GDF15 in women.
- In vitro studies using cultured human aortic endothelial cells (HAECs) treated with CRP.
- Dual-luciferase reporter assays to assess GDF15 promoter activity.
- Chromatin immunoprecipitation (ChIP) assays to determine p53 recruitment to the GDF15 promoter.
Main Results:
- A significant correlation was observed between hsCRP and GDF15 serum and mRNA levels in women.
- CRP treatment or transfection induced GDF15 expression in HAECs.
- CRP significantly enhanced GDF15 promoter activity, indicating transcriptional induction.
- CRP induced the recruitment of p53 to specific binding sites within the GDF15 promoter.
Conclusions:
- CRP induces GDF15 transcription, involving p53 recruitment to the GDF15 promoter.
- This study uncovers a novel linkage between CRP and GDF15.
- The identified CRP-GDF15 pathway may play a role in the pathogenesis of endothelial inflammation and CVD.
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