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Paracrine factors of human mesenchymal stem cells increase wound closure and reduce reactive oxygen species production in a traumatic brain injury in vitro model.

Authors
  • Torrente, D1
  • Avila, M F1
  • Cabezas, R1
  • Morales, L1
  • Gonzalez, J1
  • Samudio, I1
  • Barreto, G E2
  • 1 Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá DC, Colombia. , (Colombia)
  • 2 Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá DC, Colombia [email protected] , (Colombia)
Type
Published Article
Journal
Human & Experimental Toxicology
Publisher
SAGE Publications
Publication Date
Jul 01, 2014
Volume
33
Issue
7
Pages
673–684
Identifiers
DOI: 10.1177/0960327113509659
PMID: 24178889
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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. © The Author(s) 2014.

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