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Cell Mol Life Sci ; 75(15): 2843-2856, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29417177

RESUMO

Secondary damage following spinal cord injury leads to non-reversible lesions and hampering of the reparative process. The local production of pro-inflammatory cytokines such as TNF-α can exacerbate these events. Oligodendrocyte death also occurs, followed by progressive demyelination leading to significant tissue degeneration. Dental stem cells from human apical papilla (SCAP) can be easily obtained at the removal of an adult immature tooth. This offers a minimally invasive approach to re-use this tissue as a source of stem cells, as compared to biopsying neural tissue from a patient with a spinal cord injury. We assessed the potential of SCAP to exert neuroprotective effects by investigating two possible modes of action: modulation of neuro-inflammation and oligodendrocyte progenitor cell (OPC) differentiation. SCAP were co-cultured with LPS-activated microglia, LPS-activated rat spinal cord organotypic sections (SCOS), and LPS-activated co-cultures of SCOS and spinal cord adult OPC. We showed for the first time that SCAP can induce a reduction of TNF-α expression and secretion in inflamed spinal cord tissues and can stimulate OPC differentiation via activin-A secretion. This work underlines the potential therapeutic benefits of SCAP for spinal cord injury repair.


Assuntos
Ativinas/metabolismo , Diferenciação Celular/fisiologia , Papila Dentária/metabolismo , Inflamação/prevenção & controle , Células Precursoras de Oligodendrócitos/metabolismo , Células-Tronco/metabolismo , Adulto , Animais , Linhagem Celular , Doenças Desmielinizantes/metabolismo , Doenças Desmielinizantes/prevenção & controle , Papila Dentária/citologia , Humanos , Inflamação/metabolismo , Camundongos , Neurônios/metabolismo , Oligodendroglia/metabolismo , Ratos , Ratos Wistar , Medula Espinal/metabolismo , Traumatismos da Medula Espinal/metabolismo , Traumatismos da Medula Espinal/terapia , Células-Tronco/citologia , Fator de Necrose Tumoral alfa/metabolismo
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