Journal
JOURNAL OF BIOMEDICAL SCIENCE
Volume 23, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12929-016-0224-9
Keywords
Endoglin; Angiogenesis; Pulmonary hypertension; Microparticles
Categories
Funding
- National Institute for Health Research/Wellcome Trust Imperial Clinical Research Facility, at Imperial College Healthcare NHS Trust, London, UK
- British Heart Foundation [PG 11/13/28765]
- Ministerio de Economia y Competitividad of Spain [SAF2013-43421-R]
- FEDER funds
- British Heart Foundation [PG/12/67/29773] Funding Source: researchfish
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Background: Increased circulating levels of endoglin(+) endothelial microparticles (EMPs) have been identified in several cardiovascular disorders, related to severity. Endoglin is an auxilary receptor for transforming growth factor beta (TGF-alpha) important in the regulation of vascular structure. Results: We quantified the number of microparticles in plasma of six patients with chronic thromboembolic pulmonary hypertension (CTEPH) and age-and sex-matched pulmonary embolic (PE) and healthy controls and investigated the role of microparticle endoglin in the regulation of pulmonary endothelial function in vitro. Results show significantly increased levels of endoglin(+) EMPs in CTEPH plasma, compared to healthy and disease controls. Co-culture of human pulmonary endothelial cells with CTEPH microparticles increased intracellular levels of endoglin and enhanced TGF-beta-induced angiogenesis and Smad1,5,8 phosphorylation in cells, without affecting BMPRII expression. In an in vitro model, we generated endothelium-derived MPs with enforced membrane localization of endoglin. Co-culture of these MPs with endothelial cells increased cellular endoglin content, improved cell survival and stimulated angiogenesis in a manner similar to the effects induced by overexpressed protein. Conclusions: Increased generation of endoglin(+) EMPs in CTEPH is likely to represent a protective mechanism supporting endothelial cell survival and angiogenesis, set to counteract the effects of vascular occlusion and endothelial damage.
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