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Bouvet M, Dubois-Deruy E, Alayi TD, et al. Increased level of phosphorylated desmin and its degradation products in heart failure. Biochem Biophys Rep. 2016;6:54-62doi: 10.1016/j.bbrep.2016.02.014.
Bouvet, M., Dubois-Deruy, E., Alayi, T. D., Mulder, P., El Amranii, M., Beseme, O., Amouyel, P., Richard, V., Tomavo, S., & Pinet, F. (2016). Increased level of phosphorylated desmin and its degradation products in heart failure. Biochemistry and biophysics reports, 654-62. https://doi.org/10.1016/j.bbrep.2016.02.014
Bouvet, Marion, et al. "Increased level of phosphorylated desmin and its degradation products in heart failure." Biochemistry and biophysics reports vol. 6 (2016): 54-62. doi: https://doi.org/10.1016/j.bbrep.2016.02.014
Bouvet M, Dubois-Deruy E, Alayi TD, Mulder P, El Amranii M, Beseme O, Amouyel P, Richard V, Tomavo S, Pinet F. Increased level of phosphorylated desmin and its degradation products in heart failure. Biochem Biophys Rep. 2016 Feb 27;6:54-62. doi: 10.1016/j.bbrep.2016.02.014. eCollection 2016 Jul. PMID: 28955862; PMCID: PMC5600436.
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Biochem Biophys Rep. 2016 Feb 27;6:54-62. doi: 10.1016/j.bbrep.2016.02.014. eCollection 2016 Jul.

Increased level of phosphorylated desmin and its degradation products in heart failure.

Biochemistry and biophysics reports

Marion Bouvet, Emilie Dubois-Deruy, Tchilabalo Dilezitoko Alayi, Paul Mulder, Myriam El Amranii, Olivia Beseme, Philippe Amouyel, Vincent Richard, Stanislas Tomavo, Florence Pinet

Affiliations

  1. INSERM, U1167, University Lille, Institut Pasteur de Lille, F-59000 Lille, France.
  2. University Lille, CNRS UMR8204, INSERM, U1019, Institut Pasteur de Lille, Plateforme de Protéomique et des Peptides Modifiés (P3M), F-59000 Lille, France.
  3. INSERM, U1096, University of Rouen, Institute for Research and Innovation in Biomedicine, F-76000 Rouen, France.
  4. INSERM, U1167, University Lille, Institut Pasteur de Lille, Centre Hospitalier Régional et Universitaire de Lille, F-59000 Lille, France.

PMID: 28955862 PMCID: PMC5600436 DOI: 10.1016/j.bbrep.2016.02.014

Abstract

Although several risk factors such as infarct size have been identified, the progression/severity of heart failure (HF) remains difficult to predict in clinical practice. Using an experimental rat model of ischemic HF and phosphoproteomic technology, we found an increased level of phosphorylated desmin in the left ventricle (LV) of HF-rats. The purpose of the present work is to assess whether desmin is a circulating or only a tissue biomarker of HF. We used several antibodies in order to detect desmin, its proteolytic fragments and its phosphorylated form in LV and plasma by western blot, phosphate affinity electrophoresis, mass spectrometry and immunofluorescence. Plasma was treated with combinatorial peptide ligand library or depleted for albumin and immunoglobulins to increase the sensitivity of detection. We found a 2-fold increased serine-desmin phosphorylation in the LV of HF-rats, mainly in the insoluble fraction, suggesting the formation of desmin aggregates. Desmin cleavage products were also detected in the LV of HF rats, indicating that the increased phosphorylation of desmin results in more susceptibility to proteolytic activity, likely mediated by calpain activity. The native desmin and its degradation products were undetectable in the plasma of rat, mouse or human. These data suggest the potential of serine-phosphorylated form of desmin and its degradation products, but not of desmin itself, as tissue but not circulating biomarkers of HF.

Keywords: Desmin; Heart failure; Mass spectrometry; Phosphorylation; Plasma; Western blot

References

  1. Histochem Cell Biol. 2014 Jan;141(1):1-16 - PubMed
  2. PLoS One. 2015 Apr 23;10(4):e0119265 - PubMed
  3. Meat Sci. 2004 Nov;68(3):447-56 - PubMed
  4. Electrophoresis. 2010 Aug;31(16):2697-704 - PubMed
  5. Nat Rev Mol Cell Biol. 2014 Mar;15(3):163-77 - PubMed
  6. J Cell Mol Med. 2013 Oct;17(10):1335-44 - PubMed
  7. J Biol Chem. 2011 Oct 7;286(40):35007-19 - PubMed
  8. Circulation. 2004 Apr 6;109(13):1674-9 - PubMed
  9. J Cell Biol. 2008 Jun 2;181(5):761-75 - PubMed
  10. Circulation. 1997 Sep 16;96(6):1976-82 - PubMed
  11. FASEB J. 2008 Sep;22(9):3318-27 - PubMed
  12. Curr Opin Cell Biol. 2015 Feb;32:113-20 - PubMed
  13. Circulation. 2014 Jan 21;129(3):e28-e292 - PubMed
  14. Cardiovasc Res. 2014 Apr 1;102(1):24-34 - PubMed
  15. Proteomics. 2013 Aug;13(15):2324-34 - PubMed
  16. Circulation. 1985 Aug;72(2):406-12 - PubMed
  17. Biochim Biophys Acta. 2015 Nov;1852(11):2372-8 - PubMed
  18. Cardiovasc Res. 2015 Jul 1;107(1):56-65 - PubMed
  19. Biochim Biophys Acta. 2008 Jul-Aug;1784(7-8):1068-76 - PubMed
  20. J Biol Chem. 2007 Dec 7;282(49):35868-77 - PubMed
  21. J Intern Med. 2012 Sep;272(3):287-97 - PubMed
  22. J Mol Cell Cardiol. 2016 Oct;99:218-229 - PubMed
  23. Nat Methods. 2007 Mar;4(3):207-14 - PubMed
  24. J Proteome Res. 2008 Nov;7(11):5004-16 - PubMed
  25. J Biol Chem. 1982 May 25;257(10):5544-53 - PubMed
  26. Eur Heart J. 2011 Jan;32(1):115-23 - PubMed
  27. J Pathol. 2004 Nov;204(4):418-27 - PubMed
  28. J Mol Cell Cardiol. 2015 Jul;84:212-22 - PubMed
  29. Circulation. 2015 Sep 1;132(9):852-72 - PubMed
  30. J Am Coll Cardiol. 1998 Mar 1;31(3):645-53 - PubMed
  31. J Biol Chem. 2015 Jul 10;290(28):17145-53 - PubMed

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