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. 2018 Apr 18;9(5):444. doi: 10.1038/s41419-018-0473-5

Fig. 8. RA regulates RPC proliferation and differentiation through miR-29a.

Fig. 8

a The results of the CCK-8 analysis showed that RA induced RPC proliferation inhibition, and this trend could be partially rescued by the miR-29a inhibitor. b The qPCR analysis showed that the expression of Ki-67 was upregulated in RPCs treated with both RA and the miR-29a inhibitor compared with those only treated with RA. c The expression levels of RPC differentiation markers (β3-tubulin, rhodopsin and recoverin) were increased RA-treated RPC cultures (compared with control cultures), and miR-29a inhibitor partially reversed RA induced RPC differentiation markers upregulation. d Compared with RPCs only treated with RA, the expression levels of nestin and Pax-6 were upregulated in RPCs treated with both RA and the miR-29a inhibitor, according to the qPCR analysis. e A model of the role of REST mediated by RA in the regulation of RPC proliferation and differentiation. RA could directly degrade REST protein through the proteasome and indirectly suppress REST gene expression through the upregulation of miR-29a. Data are the averages of three independent experiments. Error bars indicate the standard deviation of the mean. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001 (Student’s t-test)