Next, lentiviral vectors were used to establish ADSCs that stably expressed ChABC. We investigated the expression of the P.
Western blotting was used to determine the relative level of ChABC expression in ChABC-ADSCs in comparison with an internal reference protein.
This process may occur through the formation of physical barriers and chemical suppression,[sup],, as well as by strongly inhibiting the formation of the nervous lateral bud.[sup] Because CSPG-mediated inhibition of nerve regeneration is mainly through the GAG side chains, it is generally believed that removing the GAG side chains or interfering with their synthesis could promote axonal regeneration.[sup] ChABC derived from actinomycetes specifically degrades the GAG side chains of most CSPGs and has been widely used in the treatment of SCI.
In this study, an LV5-CMV-GFP-EF1a-Puro-ChABC lentiviral vector was used to construct stable ADSC lines expressing ChABC. When the optimal MOI (transduction unit per cell, found to be 100) for ADSC transfection was used, GFP expression was more than 50%.
In the peripheral nervous system, axons can grow but cannot penetrate the glial scar.[sup] This study further explored the impact of ChABC intervention on the migration of ADSCs using a transwell assay.
At physiological body temperature, chABC loses half of its enzymatic activity within one hour and remaining functionality within three to five days.
Animals treated with thermostabilized chABC in combination with sustained delivery of neurotrophin-3 (a protein growth factor that helps to support the survival and differentiation of neurons) showed significant improvement in locomotor function and enhanced growth of sensory axons and sprouting of fibers for the neurotransmitter serotonin.
A recent commentary by Silver on glial scar-mediated inhibition and the inability for mammalian lesions to form growth-promoting astroglial bridges or to otherwise enhance glial-mediated regrowth articulates this issue and further elucidates the need for treatments to counteract the glial scar  such as with ChABC or others.
Enzymatic inactivation of CSPGs by ChABC renders them unable to interact with their receptors.
Because ChABC is an enzyme, it has its limitations; primarily degradation over time  and therefore requires repeated dosing to maintain adequate enzymatic activity to promote repair.
Specifically, sema3A was localized to Wisteria floribunda agglutinin- (WFA-) positive PNNs, an association that was eliminated following treatment with ChABC .
Species Model Therapeutic intervention Rat T10 complete 18 intercostal segments transection (peripheral nerve autografts (PNGs)) soaked with ChABC
and covered by FGF1-laden fibrin matrix, plus ChABC
injection in the interface of graft and host.