Muscular Dystrophy

     Muscular dystrophy (MD) is a disease characterized by progressive skeletal muscle weakness, defects in muscle proteins (dystrophin concentration is greatly reduced), and the death of muscle cells and tissue. Diagnosis is based on muscle biopsy, laboratory evaluation (increased levels of creatine phosphokinase) and EMG findings. There are nine major types of MD and most types of MD are multi-system disorders with manifestations in body systems including the heart, gastrointestinal system, nervous system, endocrine glands, eyes and brain. MD has a strong genetic link. Treatment options are limited. There has been a keen interest in using stem cells to regenerate muscle tissue and there has been success in using human stem cells for MD in mice. There is hope that adipose derived stem cells may be effective in regenerating muscle damaged by MD.

     Cell Surgical Network has developed a specific SVF deployment protocol that attempts to utilize the potential regenerative properties of SVF (rich in mesenchymal stem cells and growth factors). SVF is systemically deployed and is expected to hone to damaged areas preferentially. This is all done as an outpatient at the time of SVF harvesting and procurement. The entire cellular surgical procedure takes approximately three hours.

     We care about our Muscular Dystrophy patients at the Cell Surgical Network and take pride in the time we provide to our patients to deploy the best protocols to help our patients achieve their goals. By filling out Confidential Candidate Application, we will answer the questions and concerns you may have about Cell Surgical Network protocols for Muscular Dystrophy.


Human adipose-derived stem cell transplantation as a potential therapy for collagen VI-related congenital muscular dystrophy.
Stem Cell Res Ther. 2014 Feb 12;5(1):21. doi: 10.1186/scrt411. Alexeev V, Arita M, Donahue A, Bonaldo P, Chu ML, Igoucheva O.

INTRODUCTION: Congenital muscular dystrophies (CMD) are a clinically and genetically heterogeneous group of neuromuscular disorders characterized by muscle weakness within the first two years of life. Collagen VI-related muscle disorders have recently emerged as one of the most common types of CMD. COL6 CMD is caused by deficiency and/or dysfunction of extracellular matrix (ECM) protein collagen VI. Currently, there is no specific treatment for this disabling and life-threatening disease. The primary cellular targets for collagen VI CMD therapy are fibroblasts in muscle, tendon and skin, as opposed to muscle cells for other types of muscular dystrophies. However, recent advances in stem cell research have raised the possibility that use of adult stem cells may provide dramatic new therapies for treatment of COL6 CMD.
METHODS: Here, we developed a procedure for isolation of human stem cells from the adipose layer of neonatal skin. The adipose-derived stem cells (ADSC) were examined for expression of ECM and related genes using gene expression array analysis. The therapeutic potential of ADSC was assessed after a single intramuscular transplantation in collagen VI-deficient mice.
RESULTS: Analysis of primary cultures confirmed that established ADSC represent a morphologically homogenous population with phenotypic and functional features of adult mesenchymal stem cells. A comprehensive gene expression analysis showed that ADSC express a vast array of ECM genes. Importantly, it was observed that ADSC synthesize and secrete all three collagen VI chains, suggesting suitability of ADSC for COL6 CMD treatment. Furthermore, we have found that a single intramuscular transplantation of ADSC into Col6a1-/-Rag1-/- mice under physiological and cardiotoxin-induced injury/regeneration conditions results in efficient engraftment and migration of stem cells within the skeletal muscle. Importantly, we showed that ADSC can survive long-term and continuously secrete the therapeutic collagen VI protein missing in the mutant mice.
CONCLUSIONS: Overall, our findings suggest that stem cell therapy can potentially provide a new avenue for the treatment of COL6 CMD and other muscular disorders and injuries.
Adipose-derived stem cells enhance myogenic differentiation in the mdx mouse model of muscular dystrophy via paracrine signaling.

Neural Regen Res. 2016 Oct;11(10):1638-1643. Cao JQ, Liang YY, Li YQ1, Zhang HL1, Zhu YL2, Geng J, Yang LQ, Feng SW, Yang J, Kong J, Zhang C.

Adipose-derived stem cells have been shown to promote peripheral nerve regeneration through the paracrine secretion of neurotrophic factors. However, it is unclear whether these cells can promote myogenic differentiation in muscular dystrophy. Adipose-derived stem cells (6 × 106) were injected into the gastrocnemius muscle of mdx mice at various sites. Dystrophin expression was found in the muscle fibers. Phosphorylation levels of Akt, mammalian target of rapamycin (mTOR), eIF-4E binding protein 1 and S6 kinase 1 were increased, and the Akt/mTOR pathway was activated. Simultaneously, myogenin levels were increased, whereas cleaved caspase 3 and vimentin levels were decreased. Necrosis and fibrosis were reduced in the muscle fibers. These findings suggest that adipose-derived stem cells promote the regeneration and survival of muscle cells by inhibiting apoptosis and fibrosis, thereby alleviating muscle damage in muscular dystrophy.