PW1/Peg3 expression regulates key properties that determine mesoangioblast stem cell competence

Chiara Bonfanti, Giuliana Rossi, Francesco Saverio Tedesco, Monica Giannotta, Sara Benedetti, Rossana Tonlorenzi, Stefania Antonini, Giovanna Marazzi, Elisabetta Dejana, David Sassoon, Giulio Cossu and Graziella Messina ()
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Chiara Bonfanti: University of Milan
Giuliana Rossi: University of Milan
Francesco Saverio Tedesco: University College London
Monica Giannotta: IFOM, FIRC Institute of Molecular Oncology
Sara Benedetti: University College London
Rossana Tonlorenzi: San Raffaele Hospital
Stefania Antonini: University of Milan
Giovanna Marazzi: Stem Cells and Regenerative Medicine, ICAN UMRS 1166 Inserm/Sorbonne University (UPMC ParisVI)
Elisabetta Dejana: University of Milan
David Sassoon: Stem Cells and Regenerative Medicine, ICAN UMRS 1166 Inserm/Sorbonne University (UPMC ParisVI)
Giulio Cossu: University of Milan
Graziella Messina: University of Milan

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract Mesoangioblasts are vessel-associated progenitor cells that show therapeutic promise for the treatment of muscular dystrophy. Mesoangioblasts have the ability to undergo skeletal muscle differentiation and cross the blood vessel wall regardless of the developmental stage at which they are isolated. Here we show that PW1/Peg3 is expressed at high levels in mesoangioblasts obtained from mouse, dog and human tissues and its level of expression correlates with their myogenic competence. Silencing PW1/Peg3 markedly inhibits myogenic potential of mesoangioblasts in vitro through MyoD degradation. Moreover, lack of PW1/Peg3 abrogates mesoangioblast ability to cross the vessel wall and to engraft into damaged myofibres through the modulation of the junctional adhesion molecule-A. We conclude that PW1/Peg3 function is essential for conferring proper mesoangioblast competence and that the determination of PW1/Peg3 levels in human mesoangioblasts may serve as a biomarker to identify the best donor populations for therapeutic application in muscular dystrophies.

Date: 2015
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DOI: 10.1038/ncomms7364

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