Plasma ratio of angiopoietin-2 to angiopoietin-1 is a biomarker of vascular impairment in chronic obstructive pulmonary disease patients.


Journal

Angiogenesis
ISSN: 1573-7209
Titre abrégé: Angiogenesis
Pays: Germany
ID NLM: 9814575

Informations de publication

Date de publication:
08 2022
Historique:
received: 13 11 2021
accepted: 28 11 2021
pubmed: 12 1 2022
medline: 7 7 2022
entrez: 11 1 2022
Statut: ppublish

Résumé

Chronic obstructive pulmonary disease (COPD) patients have an increased risk of cardiovascular disease. Muscle biopsies have revealed that the muscle vasculature in COPD patients was characterized by a capillary rarefaction with reduced pericyte coverage. Thus, an imbalance of the plasma Angiopoietin-1 / Angiopoietin-2 (Ang2/Ang1) ratio could constitute a non-invasive marker of the muscle vascular impairment. In 14 COPD patients (65.5±5.1-year-old) and 7 HC (63.3±5.8-year-old), plasma samples were obtained at 3 time-points: before, after 5 weeks (W5), and after 10 weeks (W10) of exercise training. COPD patients showed a muscle capillary rarefaction at baseline with a reduced capillary coverage at W5 and W10. The plasma Ang2/Ang1 ratio was significantly higher in COPD patients vs. HC during the training (Group: p=0.01). The plasma Ang2/Ang1 ratio was inversely correlated with the pericyte coverage index regardless of the time period W0 (r=-0.51; p=0.02), W5 (r=-0.48; p=0.04), and W10 (r=-0.61; p<0.01). Last, in ECFC/MSC co-cultures exposed to the W10 serum from COPD patients and HC, the plasma Ang2/Ang1 at W10 were inversely correlated with calponin staining (r=-0.64. p=0.01 and r= 0.71. p<0.01, Fig. 1B), in line with a role of this plasma Ang2/Ang1 in the MSC differentiation into pericytes. Altogether, plasma Ang2/Ang1 ratio could constitute a potential marker of the vascular impairment in COPD patients.

Identifiants

pubmed: 35013842
doi: 10.1007/s10456-021-09826-1
pii: 10.1007/s10456-021-09826-1
doi:

Substances chimiques

Angiopoietin-1 0
Angiopoietin-2 0
Biomarkers 0

Types de publication

Letter Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

275-277

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Nature B.V.

Références

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Auteurs

Fares Gouzi (F)

INSERM - CNRS - Montpellier University, CHRU Montpellier, Montpellier, France.
Université de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.

Aurélien Philippe (A)

Université de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.
Department of Hematology and Biosurgical Research Lab (Fondation Carpentier), AP-HP, Georges Pompidou European Hospital, 20 rue Leblanc, F-75015, Paris, France.

Léo Blervaque (L)

Laboratoire Interuniversitaire de Biologie de la Motricité, Université Savoie Mont Blanc, 7424, Chambéry, EA, France.

Sven Günther (S)

Université de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.
Department of Physiology AH-HP, Georges Pompidou European Hospital, F-75015, Paris, France.

Anne Virsolvy (A)

INSERM - CNRS - Montpellier University, CHRU Montpellier, Montpellier, France.

Maxime Gruest (M)

Université de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.
Department of Hematology and Biosurgical Research Lab (Fondation Carpentier), AP-HP, Georges Pompidou European Hospital, 20 rue Leblanc, F-75015, Paris, France.

Olivier Cazorla (O)

INSERM - CNRS - Montpellier University, CHRU Montpellier, Montpellier, France.

Elisa Rossi (E)

Université de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.

David M Smadja (DM)

Université de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France. david.Smadja@aphp.fr.
Department of Hematology and Biosurgical Research Lab (Fondation Carpentier), AP-HP, Georges Pompidou European Hospital, 20 rue Leblanc, F-75015, Paris, France. david.Smadja@aphp.fr.

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