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CD20-related signaling pathway is differently activated in normal and dystrophic circulating CD133(+) stem cells

  Articoli su Riviste JCR/ISI  (anno 2009)

Autori:  Parolini, D.; Meregalli, M.; Belicchi, M.; Razini, P.; Lopa, R.; Del CarLo, B.; Farini, A.; Maciotta, S.; Bresolin, N.; Porretti, L.; Pellegrino, M.; TorDel Carlo, B.; Farini, A.; Maciotta, S.; Bresolin, N.; Porretti, L.; Pellegrino, M.; Torrente, Y

Affiliazione Autori:  Univ Milan, Ctr Dino Ferrari, Fdn IRCCS Osped Maggiore Policlin, Dept Neurol Sci,Stem Cell Lab, I-20122 Milan, Italy; Univ Milan, Ctr Interdipartimentale Ric Cellule Staminali, UNISTEM, I-20133 Milan, Italy; Fdn IRCCS Osped Maggiore Policlin, Dept Regenerat Med, Ctr Interdipartimentale Citometria, I-20122 Milan, Italy; Univ Pisa, Dept Human Physiol, I-56127 Pisa, Italy

Riassunto:  Among the heterogeneous population of circulating hematopoietic and endothelial progenitors, we identified a subpopulation of CD133(+) cells displaying myogenic properties. Unexpectedly, we observed the expression of the B-cell marker CD20 in blood-derived CD133(+) stem cells. The CD20 antigen plays a role in the modulation of intracellular calcium homeostasis through signaling pathways activation. Several observations suggest that an increase in intracellular calcium concentration ([Ca2+](i)) could be involved in the etiology of the Duchenne muscular dystrophy (DMD). Here, we show that a CD20-related signaling pathway able to induce an increase in [Ca2+](i) is differently activated after brain derived neurotrophic factor (BDNF) stimulation of normal and dystrophic blood-derived CD133(+) stem cells, supporting the assumption of a \"CD20-related calcium impairment\" affecting dystrophic cells. Presented findings represent the starting point toward the expansion of knowledge on pathways involved in the pathology of DMD and in the behavior of dystrophic blood-derived CD133(+) stem cells.

Rivista/Giornale:  CELLULAR AND MOLECULAR LIFE SCIENCES
Volume n.:  66 (4)      Pagine da: 697  a: 710
Ulteriori informazioni:  This work has been supported by the Association Monegasque contre les Myopathies (AMM), the Duchenne Parent Project de France (DPP France), and the Associazione Amici del Centro Dino Ferrari. The authors have no conflicting financial interests.
DOI: 10.1007/s00018-009-8652-2

*Impact Factor della Rivista: (2009) 6.090   *Citazioni: 6
data tratti da "WEB OF SCIENCE" (marchio registrato di Thomson Reuters) ed aggiornati a:  19/05/2019

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