Peer-Reviewed Journal Details
Mandatory Fields
Torrente, D.,Avila, M. F.,Cabezas, R.,Morales, L.,Gonzalez, J.,Samudio, I.,Barreto, G. E.
2014
July
Hum Exp Toxicolhum Exp Toxicol
Paracrine factors of human mesenchymal stem cells increase wound closure and reduce reactive oxygen species production in a traumatic brain injury in vitro model
Published
()
Optional Fields
Astrocytes/*metabolism/pathology Brain Injuries/metabolism/pathology/*surgery Cell Line, Tumor Cell Movement Cell Proliferation Cell Shape Cell Survival Culture Media, Conditioned/metabolism Down-Regulation Glioblastoma/*metabolism/pathology Glucose/deficiency Humans *Mesenchymal Stem Cell Transplantation Mesenchymal Stem Cells/*metabolism *Oxidative Stress *Paracrine Communication Signal Transduction Superoxides/*metabolism Time Factors *Wound Healing
33
77
673
84
Traumatic brain injury (TBI) consists of a primary and a secondary insult characterized by a biochemical cascade that plays a crucial role in cell death in the brain. Despite the major improvements in the acute care of head injury victims, no effective strategies exist for preventing the secondary injury cascade. This lack of success might be due to that most treatments are aimed at targeting neuronal population, even if studies show that astrocytes play a key role after a brain damage. In this work, we propose a new model of in vitro traumatic brain-like injury and use paracrine factors released by human mesenchymal stem cells (hMSCs) as a neuroprotective strategy. Our results demonstrate that hMSC-conditioned medium increased wound closure and proliferation at 12 h and reduced superoxide production to control conditions. This was accompanied by changes in cell morphology and polarity index, as both parameters reflect the ability of cells to migrate toward the wound. These findings indicate that hMSC is an important regulator of oxidative stress production, enhances cells migration, and shall be considered as a useful neuroprotective approach for brain recovery following injury.Traumatic brain injury (TBI) consists of a primary and a secondary insult characterized by a biochemical cascade that plays a crucial role in cell death in the brain. Despite the major improvements in the acute care of head injury victims, no effective strategies exist for preventing the secondary injury cascade. This lack of success might be due to that most treatments are aimed at targeting neuronal population, even if studies show that astrocytes play a key role after a brain damage. In this work, we propose a new model of in vitro traumatic brain-like injury and use paracrine factors released by human mesenchymal stem cells (hMSCs) as a neuroprotective strategy. Our results demonstrate that hMSC-conditioned medium increased wound closure and proliferation at 12 h and reduced superoxide production to control conditions. This was accompanied by changes in cell morphology and polarity index, as both parameters reflect the ability of cells to migrate toward the wound. These findings indicate that hMSC is an important regulator of oxidative stress production, enhances cells migration, and shall be considered as a useful neuroprotective approach for brain recovery following injury.
1477-0903 (Electronic) 09
2013/11/02
http://www.ncbi.nlm.nih.gov/pubmed/24178889http://www.ncbi.nlm.nih.gov/pubmed/24178889
10.1177/0960327113509659
Grant Details