Ye Dongping, Dai Libing, Yao Yicun, Qin Shengnan, Xie Han, Wang Wen, Liang Weiguo
Guangzhou City Red Cross Hospital, The Fourth Affiliated Hospital of the Medical College, Jinan University, Guangzhou 510220, China.
Dis Markers. 2016;2016:6984270. doi: 10.1155/2016/6984270. Epub 2016 Aug 18.
We first investigated the difference in microRNA expression between normal NP cells and degenerative NP cells using gene chip. We have found that the expression of ERK1/2 was decreased with overexpression of miR-155 in normal nucleus pulposus cell. Expression of ERK1/2 was increased with inhibition of miR-155. Overexpression or inhibition of miR-155 had no effects on the expression level of mRNA ERK1/2 in nucleus pulposus cell, which showed that miR-155 affected the expression of pERK1/2 after transcription of ERK1/2 mRNA indicating that ERK1/2 was a new target protein regulated by miR-155. In the degeneration of intervertebral disc, inhibited miR-155 decreased the expressions of extracellular main matrix collagen II and glycosaminoglycan and increased expression of ERK1/2. Taken together, our data suggested that miR-155 was the identified miRNA which regulated NP cells degenerated through directly targeting ERK1/2.
我们首先使用基因芯片研究了正常髓核细胞与退变髓核细胞之间微小RNA表达的差异。我们发现,在正常髓核细胞中,随着miR-155的过表达,ERK1/2的表达降低。随着miR-155的抑制,ERK1/2的表达增加。miR-155的过表达或抑制对髓核细胞中mRNA ERK1/2的表达水平没有影响,这表明miR-155在ERK1/2 mRNA转录后影响pERK1/2的表达,表明ERK1/2是受miR-155调控的新靶蛋白。在椎间盘退变过程中,抑制miR-155可降低细胞外主要基质胶原蛋白II和糖胺聚糖的表达,并增加ERK1/2的表达。综上所述,我们的数据表明,miR-155是通过直接靶向ERK1/2来调控髓核细胞退变的已鉴定微小RNA。