Activation of Wnt3a signaling promotes myogenic differentiation of mesenchymal stem cells in mdx mice.

Aim: Duchenne muscular dystrophy (DMD) is an X-linked genetic muscular disorder with no effective treatment at present. Mesenchymal stem cell (MSC) transplantation has been used to treat DMD, but the efficiency is low. Our previous studies show that activation of Wnt3a signaling promotes myogenic differentiation of MSCs in vitro.

Decorin promotes myogenic differentiation and mdx mice therapeutic effects after transplantation of rat adipose-derived stem cells.

Background Aims: Adipose-derived stem cells (ADSC) have been considered as attractive candidates for the treatment of Duchenne muscular dystrophy (DMD), but the rate of ADSC myogenesis is very low. Myostatin (Mstn), a negative regulator of myogenesis, is known to be responsible for limiting skeletal muscle regeneration. Decorin could bind Mstn and deactivate it.

Inhibition of myostatin promotes myogenic differentiation of rat bone marrow-derived mesenchymal stromal cells.

Background Aims: Mesenchymal stromal cells (MSC) have been thought to be attractive candidates for the treatment of Duchenne muscular dystrophy (DMD), but the rate of MSC myogenesis is very low. Thus MSC treatment for DMD is restricted. Myostatin (Mstn), a negative regulator of myogenesis, is known to be responsible for limiting skeletal muscle regeneration.

Neurospheres from rat adipose-derived stem cells could be induced into functional Schwann cell-like cells in vitro.

Background: Schwann cells (SC) which are myelin-forming cells in peripheral nervous system are very useful for the treatment of diseases of peripheral nervous system and central nervous system. However, it is difficult to obtain sufficient large number of SC for clinical use, so alternative cell systems are desired.

Results: Using a procedure similar to the one used for propagation of neural stem cells, we could induce rat adipose-derived stem cells (ADSC) into floating neurospheres.

Wnt3a signaling promotes proliferation, myogenic differentiation, and migration of rat bone marrow mesenchymal stem cells.

Aim: To investigate the effects of the wingless-related MMTV integration site 3A (Wnt3a) signaling on the proliferation, migration, and the myogenic and adipogenic differentiation of rat bone marrow mesenchymal stem cells (rMSC).

Methods: Primary MSC were isolated and cultured from Sprague-Dawley rats and characterized by flow cytometry. Mouse L cells were transfected with Wnt3a cDNA, and conditioned media containing active Wnt3a proteins were prepared.

Enhanced effect of microdystrophin gene transfection by HSV-VP22 mediated intercellular protein transport.

Background: Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused by mutations of dystrophin gene, there is no effective treatment for this disorder at present. Plasmid-mediated gene therapy is a promising therapeutical approach for the treatment of DMD. One of the major issues with plasmid-mediated gene therapy for DMD is poor transfection efficiency and distribution.

Herpes simplex virus VP22 enhances adenovirus-mediated microdystrophin gene transfer to skeletal muscles in dystrophin-deficient (mdx) mice.

One of the obstacles to efficient vector-mediated gene therapy for Duchenne's muscular dystrophy (DMD) is its limited transduction efficiency. The VP22 tegument protein of herpes simplex virus type 1 (HSV-1) is able to cross biological membranes and translocate the VP22 fusion protein from transfected primary cells to surrounding cells and improve the outcome of gene transfer. To improve the efficiency of vector-mediated gene therapy and to investigate the utility of the intercellular trafficking properties of VP22-linked protein for the treatment for DMD, the recombinant adenoviruses Ad-VP22, Ad-MICDYS, and Ad-VP22-MICDYS were constructed and the VP22-mediated shuttle effect was evaluated both in vitro and in vivo.