Also examination of gene expression profile of mASCs and hASCs indicated that these cells produce neurotrophic factors and myelin sheath components, which are necessary for nerve sprout outgrowth and myelination. Our study demonstrates that ability of mASCs to stimulate the growth of nerve sprouts depends on BDNF secretion. Transplantation of mASCs induces the growth of blood vessels and nerve sprouts in ischemic myocardium, stimulating regeneration. ASCs differentiated towards Schwann-like cell phenotype also promote neurite outgrowth. Furthermore, nerve conduits seeded with such cells enhance myelination and repair of Afatinib peripheral nerve. Here we demonstrate that mASCs affect the growth of tyrosine hydroxylase expressing sympathetic nerve sprouts. Furthermore, mASCs transplantation stimulated a functional recovery of crushed sensory and motor neurons, indicating that this effect is common for all nerve fibers rather than selective for particular type of neurons. In addition, nerves treated with mASCs exhibited faster structural recovery. One explanation for those effects is their ability to produce growth factors, such as VEGF, bFGF and HGF together with neurotrophins, BDNF, NGF, GDNF and NT-1. Neurotrophins stimulate nerve fiber growth and regeneration in several ways: via PI-3K or PLC-c – dependent signaling pathways ; act as positive guidance molecules for axonal growth cone, prevent apoptosis and induce proliferation of Schwann cells. Furthermore, ASCs can elevate neurotrophins production indirectly at the injury site by stimulating the growth of new blood vessels. Vascular cells produce BDNF and artemin, a neurotrophin of GDNF family, which attract growing sympathetic nerve fiber and simultaneously promote nerve fiber formation along the blood vessel. Neurotrophic activity of vascular cells attracted to the injury site by transplanted ASCs could be responsible for a longterm effect of those cells. We demonstrate that hypoxia further increases the ability of ASCs to stimulate the growth of nerve fibers. This reconciles our previous observations that low-oxygen conditions up-regulate their angiogenic capabilities and supports the idea that ASCs transplantation induces the simultaneous growth of nerve sprouts and blood vessels. Indeed, we found that in matrigel implants GAP43 positive nerve fibers which co-localized with lectin-positive blood vessels. Neural differentiation medium also increased the ability of ASCs to stimulate nerve fiber growth. Hypoxia and neural differentiation enhance the paracrine activity of ASCs. We show that low oxygen up-regulates angiogenic growth factors with modest effects on neurotrophins, and the combination of retinoic acid with 5-azacytidin further stimulates expression of neurotrophins and their secretion without influencing VEGF. Among the neurotrophins produced by ASCs, BDNF is likely to play the important role.