Abstract
Bone marrow-derived mesenchymal stem cells (BMSCs) are considered as transplants for the treatment of central nervous system (CNS) trauma, but the therapeutic effect is restricted by their finite mobility and homing capacity. Fasudil (FAS), a potent Rho kinase inhibitor, has been reported to alleviate nerve damage and induce the differentiation of BMSCs into neuron-like cells. However, the effect of FAS on the migration of BMSCs remains largely unknown. The present study revealed that FAS significantly enhanced the migration ability and actin stress fiber formation of BMSCs in vitro with an optimal concentration of 30 μmol/L. Moreover, we found that activation of the MAPK signaling pathway was involved in these FAS-mediated phenomena. In vivo, cells pretreated with FAS showed greater homing capacity from the injection site to the spinal cord injury site. Taken together, the present results indicate that FAS acts as a promoting factor of BMSC migration both in vitro and in vivo, possibly by inducing actin stress fiber formation via the MAPK signaling pathway, suggesting that FAS might possess synergistic effect in stem cell transplantation of CNS trauma.
Highlights
Spinal cord injury (SCI), a common central nervous system (CNS) trauma, causes irreversible neurological dysfunction and imposes a substantial burden on patients and their surroundings [1]
All animals were treated according to the animal guidelines of Guangzhou University of Chinese Medicine. α-Modified Eagle’s medium (α-MEM), fetal bovine serum (FBS), and trypsin were obtained from Gibco-BRL (NY, USA)
Rat bone marrow-derived mesenchymal stem cells (BMSCs) exhibited fibroblast-like shape and Primary passage 3d CD44 (97.3%)
Summary
Spinal cord injury (SCI), a common central nervous system (CNS) trauma, causes irreversible neurological dysfunction and imposes a substantial burden on patients and their surroundings [1]. Stem Cells International them, mitogen-activated protein kinase (MAPK) is the main signaling pathway of cellular motility, proliferation, and apoptosis, which is involved in the maintenance of neuronal hyperexcitability after SCI [13,14,15]. These findings provide more direction for future clinical treatment. By suppressing with FAS, it is possible to block the inhibitory effects of Rho/ROCK pathway during regeneration and normalize the blood flow of the injured sites, thereby further protecting damaged nerve tissues [19]. Our findings provide a theoretical basis for FAS to play a promising role in stem cell transplantation for CNS trauma
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
