Literature DB >> 27742621

TSP1-CD47 signaling is upregulated in clinical pulmonary hypertension and contributes to pulmonary arterial vasculopathy and dysfunction.

Natasha M Rogers1,2,3, Maryam Sharifi-Sanjani1, Mingyi Yao4, Kedar Ghimire1, Raquel Bienes-Martinez1, Stephanie M Mutchler5, Heather E Knupp1, Jeffrey Baust1, Enrico M Novelli1, Mark Ross6, Claudette St Croix6, Johannes C Kutten1, Caitlin A Czajka1, John C Sembrat7,8, Mauricio Rojas7,8, David Labrousse-Arias9, Timothy N Bachman1, Rebecca R Vanderpool1, Brian S Zuckerbraun10, Hunter C Champion1,7, Ana L Mora1,7, Adam C Straub1,5, Richard A Bilonick11, Maria J Calzada9, Jeffrey S Isenberg12,5,7.   

Abstract

AIMS: Thrombospondin-1 (TSP1) is a ligand for CD47 and TSP1-/- mice are protected from pulmonary hypertension (PH). We hypothesized the TSP1-CD47 axis is upregulated in human PH and promotes pulmonary arterial vasculopathy. METHODS AND
RESULTS: We analyzed the molecular signature and functional response of lung tissue and distal pulmonary arteries (PAs) from individuals with (n = 23) and without (n = 16) PH. Compared with controls, lungs and distal PAs from PH patients showed induction of TSP1-CD47 and endothelin-1/endothelin A receptor (ET-1/ETA) protein and mRNA. In control PAs, treatment with exogenous TSP1 inhibited vasodilation and potentiated vasoconstriction to ET-1. Treatment of diseased PAs from PH patients with a CD47 blocking antibody improved sensitivity to vasodilators. Hypoxic wild type (WT) mice developed PH and displayed upregulation of pulmonary TSP1, CD47, and ET-1/ETA concurrent with down regulation of the transcription factor cell homolog of the v-myc oncogene (cMyc). In contrast, PH was attenuated in hypoxic CD47-/- mice while pulmonary TSP1 and ET-1/ETA were unchanged and cMyc was overexpressed. In CD47-/- pulmonary endothelial cells cMyc was increased and ET-1 decreased. In CD47+/+ cells, forced induction of cMyc suppressed ET-1 transcript, whereas suppression of cMyc increased ET-1 signaling. Furthermore, disrupting TSP1-CD47 signaling in pulmonary smooth muscle cells abrogated ET-1-stimulated hypertrophy. Finally, a CD47 antibody given 2 weeks after monocrotaline challenge in rats upregulated pulmonary cMyc and improved aberrations in PH-associated cardiopulmonary parameters.
CONCLUSIONS: In pre-clinical models of PH CD47 targets cMyc to increase ET-1 signaling. In clinical PH TSP1-CD47 is upregulated, and in both, contributes to pulmonary arterial vasculopathy and dysfunction. Published on behalf of the European Society of Cardiology. All rights reserved.
© The Author 2016. For Permissions, please email: journals.permissions@oup.com.

Entities:  

Keywords:  CD47; Clinical pulmonary hypertension; ET-1; Thrombospondin-1; cMyc

Mesh:

Substances:

Year:  2016        PMID: 27742621      PMCID: PMC5220673          DOI: 10.1093/cvr/cvw218

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  70 in total

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