Exendin-4 promotes actin cytoskeleton rearrangement and protects cells from Nogo-A-Δ20 mediated spreading inhibition and growth cone collapse by down-regulating RhoA expression and activation via the PI3K pathway - 09/12/18
, Xuyi Chen c, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Highlights |
• | Exendin-4 increases phosphorylation of cofilin and promotes actin cytoskeleton rearrangement. |
• | Exendin-4 protects SH-SY5Y and PC12 cells from Nogo-A-Δ20-mediated spreading inhibition. |
• | Exendin-4 induces SH-SY5Y differentiation and reduces Nogo-A-Δ20-mediated growth cone collapse. |
• | Exendin-4 significantly reduce SH-SY5Y cell migration. |
• | Exendin-4 decreases the expression and activation of RhoA/Rock1 via PI3K signaling pathway. |
Abstract |
Exendin-4 is a protein of the GLP-1 family currently used to treat diabetes. Recently, a greater number of biological properties have been associated with the GLP-1 family. Our data shows that exendin-4 treatment significantly increases the cytoskeleton rearrangement, which leads to an increasingly differentiated phenotype and reduced cell migration. We also found that exendin-4 could prevent SH-SY5Y and PC12 cells from Nogo-A-Δ20 mediated spreading inhibition and neurite collapse. Western blot analysis indicated that exendin-4 treatment both reduced the expression and activation of RhoA via the PI3K signaling pathway. These data suggest that exendin-4 may protect nerve regeneration by preventing the inhibition of Nogo-A via down-regulating RhoA expression and activation.
Le texte complet de cet article est disponible en PDF.Keywords : Exendin-4, Nogo-A-Δ20, RhoA, Cell spreading, Growth cone, Cell migration
Plan
Vol 109
P. 135-143 - janvier 2019 Retour au numéro
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