Decreased miR-187 induces retinal ganglion cell apoptosis through upregulating SMAD7 in glaucoma - 12/10/15
, Tian-Zi Zhang a, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Background |
Retinal ganglion cells (RGCs) are commonly experienced optic nerve diseases including glaucoma-induced injury that results in decrease of cell survival. However, the underlying mechanism remains to be elaborated. This present study was to focus on the miR-187 and Transforming growth factor-β (TGF-β) signal and investigated their roles in RGCs apoptosis and proliferation.
Methods |
RGC-5 retinal ganglion cell line was chose in present study and subjected to miR-187 mimic or inhibitor transfection. Cell apoptosis was evaluated using flow cytometry-based Annexin V-PI assay. Cell proliferation was examined using CCK-8. Protein levels of Smad2/3/7 were determined using western blotting.
Results |
miR-187 negatively regulated cell survival via inhibiting cell apoptosis and promoting cell proliferation. We observed that alteration expression of miR-187 is closely related to phosphorylation levels of Smad2 and Smad3. This correlation is associated with down-regulation of Smad7 induced by miR-187 via targeting Smad7 3’-UTR. From result of co-transfection of Smad7-plasmid and miR-187 mimic or siSmad7 and miR-187 inhibitor, we concluded that cell proliferation and apoptosis was mediated by miR-187/Smad7 axis.
Conclusion |
In summary, cell internal signal transduction, miR-187 regulating Smad7 expression, plays a vital role in retinal ganglion cell survival.
Le texte complet de cet article est disponible en PDF.Keywords : Smad2, Smad3, RGC-5, TGF-β, CCK-8
Plan
Vol 75
P. 19-25 - octobre 2015 Retour au numéro
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