A novel p38 mitogen-activated protein kinase/Elk-1 transcription factor-dependent molecular mechanism underlying abnormal endothelial cell proliferation in plexogenic pulmonary arterial hypertension

Monal Patel, Dan Predescu, Rajive Tandon, Cristina Bardita, Jennifer Pogoriler, Sangeeta Bhorade, Minhua Wang, Suzy Comhair, Anna Ryan-Hemnes, Jiwang Chen, Roberto Machado, Aliya Husain, Serpil Erzurum, Sanda Predescu*

*Corresponding author for this work

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Background: Plexiform lesions comprising proliferative endothelial cells are hallmarks of pulmonary arterial hypertension. Results: Granzyme B cleaves intersectin-1s and generates a fragment with endothelial cell proliferative potential via phosphorylation of p38MAPK and Elk-1 transcription factor. Conclusion: Granzyme B cleavage of intersectin-1s and subsequent p38MAPK/Elk-1 activation are critical for endothelial cell proliferation. Significance: The novel pathogenic p38MAPK/Elk-1 signaling may explain the formation of plexiform lesions.

Original languageEnglish (US)
Pages (from-to)25701-25716
Number of pages16
JournalJournal of Biological Chemistry
Volume288
Issue number36
DOIs
StatePublished - Sep 6 2013

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Patel, M., Predescu, D., Tandon, R., Bardita, C., Pogoriler, J., Bhorade, S., Wang, M., Comhair, S., Ryan-Hemnes, A., Chen, J., Machado, R., Husain, A., Erzurum, S., & Predescu, S. (2013). A novel p38 mitogen-activated protein kinase/Elk-1 transcription factor-dependent molecular mechanism underlying abnormal endothelial cell proliferation in plexogenic pulmonary arterial hypertension. Journal of Biological Chemistry, 288(36), 25701-25716. https://doi.org/10.1074/jbc.M113.502674