HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Autologous adipose-derived stem cells attenuate muscular atrophy and protect spinal cord ventral horn motor neurons in an animal model of burn injury.

AbstractBACKGROUND AIMS:
Burn injuries might increase muscle mass loss, but the mechanisms are still unclear. In this study, we demonstrated that burn injury induced spinal cord ventral horn motor neuron (VHMN) 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 a 75°C metal surface for 10 seconds. Adipose tissues were harvested from the groin fat pad, expanded in culture and labeled with chloromethyl-benzamido/1,1'-dioctadecyl-3,3,3',3'- tetramethyl indocarbocyanine perchlorate. 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 terminal deoxynucleotidyl transferase (TUNEL) assay, caspase-3, caspase-9, CD 90 and S100, and the gastrocnemius muscle was evaluated through the use of hematoxylin and eosin staining.
RESULTS:
Caspase-3-positive, caspase-9-positive 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.
CONCLUSIONS:
The animal model of third-degree burns in the hind paw showed significant apoptosis in the corresponding spinal cord VHMNs, which suggests that neuroprotection might be the potentially therapeutic target in burn-induced muscle atrophy. ASCs have potential neuroprotection against burn injuries through its anti-apoptotic effects.
AuthorsSheng-Hua Wu, Shu-Hung Huang, Yi-Ching Lo, Chee-Yin Chai, Su-Shin Lee, Kao-Ping Chang, Sin-Daw Lin, Chung-Sheng Lai, Jwu-Lai Yeh, Aij-Lie Kwan
JournalCytotherapy (Cytotherapy) Vol. 17 Issue 8 Pg. 1066-75 (Aug 2015) ISSN: 1477-2566 [Electronic] England
PMID26139546 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2015. Published by Elsevier Inc.
Chemical References
  • Antigens, CD
  • Caspases
Topics
  • Adipocytes (cytology)
  • Adipose Tissue (cytology)
  • Animals
  • Antigens, CD (metabolism)
  • Apoptosis (physiology)
  • Burns (pathology, therapy)
  • Caspases (metabolism)
  • Disease Models, Animal
  • In Situ Nick-End Labeling
  • Male
  • Motor Neurons (pathology)
  • Muscle, Skeletal (pathology)
  • Muscular Atrophy (pathology, prevention & control, therapy)
  • Neuroprotection
  • Rats
  • Rats, Sprague-Dawley
  • Schwann Cells (pathology)
  • Sciatic Nerve (cytology, pathology)
  • Spinal Cord Ventral Horn (pathology)
  • Stem Cell Transplantation
  • Stem Cells (cytology)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: