Autologous adipose-derived stem cells attenuates muscular atrophy and protects the spinal cord ventral horn motor neuron in an animal model of burn injury

Autologous adipose-derived stem cells attenuates muscular atrophy and protects the spinal cord ventral horn motor neuron in an animal model of burn injury

Shu-Hung Huang^1.2.3.4, Su-Shin Lee^2.3.4; Kao-Ping Chang^3.4 ; Sin-Daw Lin ^3.4; Chung-Sheng Lai^2.3.4

 

1.Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan ;

2. Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung, Taiwan ;

3.Division of Plastic Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan

4. Department of Surgery, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

 

 

Background:

Burn injuries might increase muscle mass loss, but the mechanisms are still unclear. In this study, we demonstrated that burn injury induced spinal cord VHMNs apoptosis and subsequently caused muscle atrophy, and revealed the potential protection of autologous adipose-derived stem cells (ASCs) transplantation on spinal cord VHMNs and muscle against burn injury.  

Methods:

Third-degree hind-paw burns were established by contact with 75 °C metal surface for 10 seconds. Adipose tissues were harvest from groin fat pad, expanded in culture and labeled with CM-DiI. The ASCs were transplanted into the injured hind paw at 4 weeks after burn injury. The lumbar spinal cord, sciatic nerve, gastrocnemius muscle, and hind-paw skin were processed for immunofluorescent staining at 4 weeks after transplantation, including TUNEL assay, caspase-3, caspase-9, CD 90 and S100, and the gastrocnemius muscle was evaluated using hematoxylin-eosin staining.

Results:

Caspase-3, caspase-9 and TUNEL-positive cells were significantly increased in the corresponding dermatome spinal cord VHMNs after burn injury. Moreover, the decrease of Schwann cells in sciatic nerve and the increase of denervation atrophy in gastrocnemius muscle were observed.  Furthermore, ASCs transplantation significantly attenuated apoptotic death of VHMNs and the area of muscle denervation atrophy in the gastrocnemius muscle fibers.

Conclusion:

 The animal model of third-degree burns in the hind paw showed the significant apoptosis in the corresponding spinal cord VHMNs, suggesting neuroprotection might be the potentially therapeutic target in burn-induce muscle atrophy. ASCs possess potential neuroprotection against burn injury via its anti-apoptotic effects.