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Transplantation of Induced Pluripotent Stem Cell-derived Mesoangioblast-like Myogenic Progenitors in Mouse Models of Muscle Regeneration
Published on: January 20, 2014
CCR2 improves homing and engraftment of adipose-derived stem cells in dystrophic mice
Liang Wang1,2, Huan Li1,2, Jinfu Lin1,2
1Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, GD, China.
Background:
Dystrophinopathy, a common neuromuscular disorder caused by the absence of dystrophin, currently lacks effective treatments. Systemic transplantation of adipose-derived stem cells (ADSCs) is a promising treatment approach, but its low efficacy remains a challenge. Chemokine system-mediated stem cell homing plays a critical role in systemic transplantation. Here, we investigated whether overexpression of a specific chemokine receptor could improve muscle homing and therapeutic effects of ADSC systemic transplantation in dystrophic mice.
Methods:
We analysed multiple microarray datasets from the Gene Expression Omnibus to identify a candidate chemokine receptor and then evaluated the protein expression of target ligands in different tissues and organs of dystrophic mice. The candidate chemokine receptor was overexpressed using the lentiviral system in mouse ADSCs, which were used for systemic transplantation into the dystrophic mice, followed by evaluation of motor function, stem cell muscle homing, dystrophin expression, and muscle pathology.
Results:
Chemokine-profile analysis identified C-C chemokine receptor (CCR)2 as the potential target for improving ADSC homing. We found that the levels of its ligands C-C chemokine ligand (CCL)2 and CCL7 were higher in muscles than in other tissues and organs of dystrophic mice. Additionally, CCR2 overexpression improved ADSC migration ability and maintained their multilineage-differentiation potentials. Compared with control ADSCs, transplantation of those overexpressing CCR2 displayed better muscle homing and further improved motor function, dystrophin expression, and muscle pathology in dystrophic mice.
Conclusions:
These results demonstrated that CCR2 improved ADSC muscle homing and therapeutic effects following systemic transplantation in dystrophic mice.
Insights
Overexpressing chemokine receptor CCR2 in adipose-derived stem cells (ADSCs) significantly improved their homing to muscles in dystrophic mice, enhancing motor function and disease pathology.
Area of Science:
- Regenerative Medicine
- Stem Cell Biology
- Neuromuscular Disorders
Background:
- Dystrophinopathy, a neuromuscular disorder, lacks effective treatments.
- Systemic adipose-derived stem cell (ADSC) transplantation shows promise but has low efficacy.
- Chemokine-mediated stem cell homing is crucial for successful transplantation.
Purpose of the Study:
- To investigate if overexpressing a chemokine receptor can enhance ADSC muscle homing and therapeutic effects.
- To identify a specific chemokine receptor for improving ADSC homing in dystrophic models.
Main Methods:
- Analyzed microarray data to identify candidate chemokine receptors.
- Overexpressed the candidate receptor (CCR2) in mouse ADSCs using lentiviral vectors.
- Transplanted modified ADSCs into dystrophic mice and evaluated motor function, muscle homing, dystrophin expression, and pathology.
Main Results:
- C-C chemokine receptor (CCR2) was identified as a target for improving ADSC homing.
- CCR2 ligands (CCL2, CCL7) were elevated in dystrophic mouse muscles.
- CCR2 overexpression enhanced ADSC migration and differentiation potential.
- Transplanted CCR2-overexpressing ADSCs showed improved muscle homing, motor function, and reduced pathology.
Conclusions:
- CCR2 overexpression enhances ADSC muscle homing.
- CCR2-modified ADSC transplantation improves therapeutic outcomes in dystrophic mice.
