Whereas when the cells were cultured under hypoxic conditions we found only an increase of BDNF mRNA. This observation might be explained by the fact that production of BDNF protein is regulated at the level of translation. Thus, the long BDNF 39UTR has been reported as a bona fide cisacting translation suppressor of BDNF mRNA. Furthermore, BDNF translation is also regulated by microRNA, e.g. miR-30a5p targets specific sequences surrounding the proximal polyadenylation site within BDNF 39-untranslated region and overexpression of this miR results in down-regulation of BDNF protein. Thus, prevention of hypoxia-induced brain damage by conditioned medium from ASCs has been attributed to BDNF secretion. Furthermore, adenoviruses encoding BDNF have been used to stimulate axonal regeneration. We demonstrate that the ability of ASCs to up-regulate nerve sprouts growth correlates with their production of BDNF and that anti-BDNF neutralizing antibodies abrogated their stimulatory effect, indicating that BDNF is an important mediator of ASCs actions. Growing nerve sprouts migrate along specific matrix components, including laminins. Just like bone marrow-derived MSCs, ASCs also express AB1010 several genes of the laminin family, indicating that these cells can directly support growing nerve sprouts. Thus, ASCs play a role analogous to Schwann cells at sites of transplantation. Interestingly, transcriptome analysis revealed the expression of neural marker genes by ASCs, including nestin, beta3-tubulin and neurofilament 150. Furthermore, these cells appeared to express myelination master-gene Krox20 and its transcriptional targets, major components of myelin sheath. While this manuscript was in preparation a study was published showing that MSCs derived from bone marrow and adipose tissue express mRNAs encoding several myelin components and co-culture with neural cells stimulates the secretion of these proteins. Our functional and histological data suggest that faster healing of crushed common peroneal nerve is due at least in part to restoration or protection of the myelin sheath by mASCs application. Either contact with injured nerves or neural differentiation medium triggers the myelination program by ASCs. The reason as to why ASCs exhibit an expression profile similar to Schwann cells might be due to their similar embryonic origin. This clearly requires further study. Taken together, our data suggest that ASCs similar to Schwann cells can provide neurotrophic growth factors to injured nerves and improving their re-myelination. Incubation in hypoxic conditions or in neural differentiation medium prior to transplantation increases their regenerative potential, which depends on the production of neurotrophins, particularly BDNF. Therefore, ASCs might be a useful cell therapy for regeneration of injured peripheral nerves and their re-myelination.