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Plasma proteomics of differential outcome to long-term therapy in children with idiopathic pulmonary arterial hypertension
Article first published online: 29 JUN 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
PROTEOMICS - Clinical Applications
Volume 6, Issue 5-6, pages 257–267, June 2012
How to Cite
Yeager, M. E., Colvin, K. L., Everett, A. D., Stenmark, K. R. and Ivy, D. D. (2012), Plasma proteomics of differential outcome to long-term therapy in children with idiopathic pulmonary arterial hypertension. Prot. Clin. Appl., 6: 257–267. doi: 10.1002/prca.201100078
- Issue published online: 29 JUN 2012
- Article first published online: 29 JUN 2012
- Accepted manuscript online: 1 JUN 2012 04:48AM EST
- Manuscript Accepted: 7 FEB 2012
- Manuscript Revised: 2 JAN 2012
- Manuscript Received: 6 SEP 2011
- National Institutes of Health (NIH) Specialized Centers of Clinically Oriented Research (SCCOR). Grant Number: HL-084923-02
- NIH. Grant Number: HL-014985-35
- Jayden DeLuca Foundation. Grant Number: M01-RR00069
- Pulmonary hypertension;
The prognosis for children with IPAH unresponsive to therapy is poor. We investigated the plasma proteome for a molecular basis of good versus poor outcome to long-term vasodilator therapy.
Plasma was collected at baseline or shortly after therapy initiation and following chronic vasodilator therapy, then divided into those with good outcome (n = 8), and those with a poor outcome (n = 7). To identify proteins unique to either outcome, we used differential gel electrophoresis and mass spectrometry. Results were confirmed by commercial enzyme-linked immunosorbent assay.
Before and after therapy, SAA-4 was 4-fold lower in those with good outcome compared to those with poor outcome, while serum paraoxonase/arylesterase-1 was increased 2-fold in those with good outcome versus poor outcome. After therapy, haptoglobin and hemopexin were 1.45- and 1.8-fold lower, respectively, in those with a good versus poor outcome. Among those with a good outcome, SAP was 1.3-fold lower prior to therapy.
Conclusions and clinical relevance
SAP and SAA-4 regulate circulating mononuclear phagocytes. As such, they may contribute to the differential response to chronic vasodilator therapy in the context of inflammation in IPAH.