Embryonic VE-Cadherin-expressing progenitors (eVE-Cad+), including hemogenic endothelium, have been shown to generate hematopoietic stem cells and a variety of other progenitors, including mesoangioblasts, or MABs. MABs are vessel-associated progenitors with multilineage mesodermal differentiation potential that can physiologically contribute to skeletal muscle development and regeneration, and have been used in an ex vivo cell therapy setting for the treatment of muscular dystrophy. There is currently a therapeutic need for molecules that could improve the efficacy of cell therapy protocols; one such good candidate is nitric oxide. Several studies in animal models of muscle dystrophy have demonstrated that nitric oxide donors provide several beneficial effects, including modulation of the activity of endogenous cell populations involved in muscle repair and the delay of muscle degeneration. Here we used a genetic lineage tracing approach to investigate whether the therapeutic effect of nitric oxide in muscle repair could derive from an improvement in the myogenic differentiation of eVE-Cad+ progenitors during embryogenesis. We show that early in vivo treatment with the nitric oxide donor molsidomine enhances eVE-Cad+ contribution to embryonic and fetal myogenesis, and that this effect could originate from a modulation of the properties of yolk sac hemogenic endothelium.

Tirone, M., Conti, V., Manenti, F., Nicolosi, P., D'Orlando, C., Azzoni, E., et al. (2016). Nitric oxide donor molsidomine positively modulates myogenic differentiation of embryonic endothelial progenitors. PLOS ONE, 11(10) [10.1371/journal.pone.0164893].

Nitric oxide donor molsidomine positively modulates myogenic differentiation of embryonic endothelial progenitors

TIRONE, MARIO
Primo
;
CONTI, VALENTINA
Secondo
;
NICOLOSI, PIER ANDREA;D'ORLANDO, CRISTINA;Azzoni, E
;
BRUNELLI, SILVIA
Ultimo
2016

Abstract

Embryonic VE-Cadherin-expressing progenitors (eVE-Cad+), including hemogenic endothelium, have been shown to generate hematopoietic stem cells and a variety of other progenitors, including mesoangioblasts, or MABs. MABs are vessel-associated progenitors with multilineage mesodermal differentiation potential that can physiologically contribute to skeletal muscle development and regeneration, and have been used in an ex vivo cell therapy setting for the treatment of muscular dystrophy. There is currently a therapeutic need for molecules that could improve the efficacy of cell therapy protocols; one such good candidate is nitric oxide. Several studies in animal models of muscle dystrophy have demonstrated that nitric oxide donors provide several beneficial effects, including modulation of the activity of endogenous cell populations involved in muscle repair and the delay of muscle degeneration. Here we used a genetic lineage tracing approach to investigate whether the therapeutic effect of nitric oxide in muscle repair could derive from an improvement in the myogenic differentiation of eVE-Cad+ progenitors during embryogenesis. We show that early in vivo treatment with the nitric oxide donor molsidomine enhances eVE-Cad+ contribution to embryonic and fetal myogenesis, and that this effect could originate from a modulation of the properties of yolk sac hemogenic endothelium.
Articolo in rivista - Articolo scientifico
Embryos, Nitric oxide , Muscle differentiation, Yolk sac, Endothelium
English
2016
11
10
e0164893
open
Tirone, M., Conti, V., Manenti, F., Nicolosi, P., D'Orlando, C., Azzoni, E., et al. (2016). Nitric oxide donor molsidomine positively modulates myogenic differentiation of embryonic endothelial progenitors. PLOS ONE, 11(10) [10.1371/journal.pone.0164893].
File in questo prodotto:
File Dimensione Formato  
10281-133851.pdf

accesso aperto

Tipologia di allegato: Publisher’s Version (Version of Record, VoR)
Dimensione 2.73 MB
Formato Adobe PDF
2.73 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/133851
Citazioni
  • Scopus 7
  • ???jsp.display-item.citation.isi??? 4
Social impact