BACKGROUND: miR-138 is one of the down-regulated miRNAs during acute spinal cord injury. Mixed lineage kinase 3 (MLK3), a key factor of jun N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) pathway, is the target of miR-138. The aim of this study was to investigate the role of miR-138 in H2O2-treated BV-2 cells. METHODS: Murine microglia BV-2 cells were treated with H2O2 and tested for cell viability and miR-138 expression. The cells were then transfected with miR-138 agomir or miR-138 antagomir, and treated with 200 μM H2O2 for 24 h. The cellular apoptosis was detected by Aennexin V/PI staining. Expression of miR-138, MLK3, and other factors of JNK/MAPK pathway was detected. RESULTS: After treatment of various concentrations of H2O2, the cell viabilities were reduced, and miR-138 expression was down-regulated. Compared to the control cells, over-expressing miR-138 in BV-2 cells reduced apoptosis rate from 24.2 % to 11.9 %. Western blot further showed that JNK, p-JNK, c-jun, p-c-jun, p38 MAPK, and p-p38 MAPK were down-regulated. Expression of pro-apoptosis factors iNOS and COX-2 were also down-regulated. Transfection of miR-138 antagomir produced the opposite effect of the transfection of miR-138 agomir. CONCLUSION: miR-138 was able to reduce H2O2-induced apoptosis in BV-2 cells. The protective effect was related to the down-regulation of MLK3 proteins and sequentially inhibiting JNK/MAPK signaling pathway (Fig. 3, Ref. 27). Text in PDF www.elis.sk.
BACKGROUND:miR-138 is one of the down-regulated miRNAs during acute spinal cord injury. Mixed lineage kinase 3 (MLK3), a key factor of jun N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) pathway, is the target of miR-138. The aim of this study was to investigate the role of miR-138 in H2O2-treated BV-2 cells. METHODS:Murine microglia BV-2 cells were treated with H2O2 and tested for cell viability and miR-138 expression. The cells were then transfected with miR-138 agomir or miR-138 antagomir, and treated with 200 μM H2O2 for 24 h. The cellular apoptosis was detected by Aennexin V/PI staining. Expression of miR-138, MLK3, and other factors of JNK/MAPK pathway was detected. RESULTS: After treatment of various concentrations of H2O2, the cell viabilities were reduced, and miR-138 expression was down-regulated. Compared to the control cells, over-expressing miR-138 in BV-2 cells reduced apoptosis rate from 24.2 % to 11.9 %. Western blot further showed that JNK, p-JNK, c-jun, p-c-jun, p38 MAPK, and p-p38 MAPK were down-regulated. Expression of pro-apoptosis factors iNOS and COX-2 were also down-regulated. Transfection of miR-138 antagomir produced the opposite effect of the transfection of miR-138 agomir. CONCLUSION:miR-138 was able to reduce H2O2-induced apoptosis in BV-2 cells. The protective effect was related to the down-regulation of MLK3 proteins and sequentially inhibiting JNK/MAPK signaling pathway (Fig. 3, Ref. 27). Text in PDF www.elis.sk.
Authors: Laura Baumgartner; Karin Wuertz-Kozak; Christine L Le Maitre; Francis Wignall; Stephen M Richardson; Judith Hoyland; Carlos Ruiz Wills; Miguel A González Ballester; Michael Neidlin; Leonidas G Alexopoulos; Jérôme Noailly Journal: Int J Mol Sci Date: 2021-01-12 Impact factor: 5.923
Authors: Rodrigo M Maza; María Asunción Barreda-Manso; David Reigada; Ágata Silván; Teresa Muñoz-Galdeano; Altea Soto; Ángela Del Águila; Manuel Nieto-Díaz Journal: Biomedicines Date: 2022-06-30