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Updated: Jun 26, 2026

Isolation of CD133+ Liver Stem Cells for Clonal Expansion
Published on: October 10, 2011
CD20-related signaling pathway is differently activated in normal and dystrophic circulating CD133(+) stem cells
D Parolini1, M Meregalli, M Belicchi
1Department of Neurological Sciences, Fondazione IRCCS Ospedale Maggiore Policlinico, Centro Dino Ferrari, University of Milan, Italy.
Insights
Researchers found a CD20-related signaling pathway that affects calcium levels in blood stem cells. This pathway is altered in Duchenne muscular dystrophy (DMD), suggesting a new target for understanding this disease.
Area of Science:
- Biomedical Science
- Stem Cell Biology
- Molecular Medicine
Background:
- Circulating CD133(+) stem cells possess myogenic properties.
- The B-cell marker CD20 is unexpectedly expressed on blood-derived CD133(+) stem cells.
- CD20 signaling influences intracellular calcium homeostasis, a factor implicated in Duchenne muscular dystrophy (DMD).
Purpose of the Study:
- To investigate the role of CD20 signaling in blood-derived CD133(+) stem cells.
- To explore the potential link between CD20, calcium regulation, and DMD.
- To compare the activation of CD20-related pathways in normal and dystrophic stem cells.
Main Methods:
- Identification and characterization of CD133(+) stem cell subpopulations.
- Analysis of CD20 expression on blood-derived stem cells.
- Stimulation with brain-derived neurotrophic factor (BDNF) and measurement of intracellular calcium ([Ca(2+)](i)) changes.
Main Results:
- A subpopulation of CD133(+) cells with myogenic properties was identified.
- CD20 expression was observed on blood-derived CD133(+) stem cells.
- A CD20-related signaling pathway inducing [Ca(2+)](i) increase showed differential activation between normal and dystrophic stem cells upon BDNF stimulation.
Conclusions:
- Findings suggest a "CD20-related calcium impairment" in dystrophic cells.
- This study provides a foundation for understanding DMD pathology and dystrophic stem cell behavior.
- Highlights potential pathways involved in DMD etiology and stem cell dysfunction.
Abstract:
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 ([Ca(2+)](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 [Ca(2+)](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.
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