Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkIIδ.
Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkIIδ.
复制标题
视黄酸诱导的 microRNA-31-5p 通过靶向 CamkII delta 抑制肌原性增殖和分化
DOI：
10.1186/s13395-017-0126-x
复制
发表时间：
2017-05-11
期刊：
影响因子：
4.9
通讯作者：
Xiao J
中科院分区：
文献类型：
--
作者：
Liu B;Liu C;Cong W;Li N;Zhou N;Tang Y;Wei C;Bai H;Zhang Y;Xiao J
我们之前报道过Wnt5a/CaMKIIδ（钙/钙调素依赖性蛋白激酶IIδ）通路参与过量维甲酸（RA）诱导的胚胎舌畸形。我们的最新研究发现，在ra处理的胚胎舌中，miR-31-5p的表达升高，miR-31-5p被预测靶向CamkIIδ的3'UTR。因此，我们假设在胚胎舌中过量的RA通过miR-31-5p调控Wnt5a/CaMKIIδ通路。我们以C2C12成肌细胞系为体外模型，研究了miR-31-5p对CamkIIδ表达的抑制作用，RA通过其抑制胚胎舌成肌细胞的增殖和分化。RA刺激了miR-31-5p在胚胎舌细胞和C2C12成肌细胞中的表达。荧光素酶报告基因检测证实CamkIIδ的3'UTR是miR-31-5p的靶标。MiR-31-5p模拟物与过量RA一样破坏CamkIIδ表达、C2C12增殖和分化，而MiR-31-5p抑制剂在RA存在时部分挽救了这些缺陷。过量的RA可刺激miR-31-5p表达抑制CamkIIδ，从而抑制舌成肌细胞的增殖和分化。本文的在线版本（doi:10.1186/s13395-017-0126-x）包含补充材料，可供授权用户使用。
We previously reported that Wnt5a/CaMKIIδ (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Our latest study found that the expression of miR-31-5p, which was predicted to target the 3′UTR of CamkIIδ, was raised in the RA-treated embryonic tongue. Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKIIδ pathway through miR-31-5p in embryonic tongue. C2C12 myoblast line was employed as an in vitro model to examine the suppression of miR-31-5p on CamkIIδ expression, through which RA impaired the myoblast proliferation and differentiation in embryonic tongue. RA stimulated the expression of miR-31-5p in both embryonic tongue and C2C12 myoblasts. Luciferase reporter assay confirmed that the 3′UTR of CamkIIδ was a target of miR-31-5p. MiR-31-5p mimics disrupted CamkIIδ expression, C2C12 proliferation and differentiation as excess RA did, while miR-31-5p inhibitor partially rescued these defects in the presence of RA. Excess RA can stimulate miR-31-5p expression to suppress CamkIIδ, which represses the proliferation and differentiation of tongue myoblasts. The online version of this article (doi:10.1186/s13395-017-0126-x) contains supplementary material, which is available to authorized users.