LncRNA H19/Runx2 axis promotes VSMCs transition via MAPK pathway.

Arterial calcification (AC) is mainly caused by osteoblast phenotypic transition of vascular smooth muscle cells (VSMCs). Long noncoding RNA H19 (lncRNA H19) has attracted increasingly attention because of their transcriptional regulation crucial potency. We reported that lncRNA H19 expression is up-regulated after VSMCs transition. Thus, we aim to study the role of H19 and the molecular mechanisms in VSMCs transition. To determine the expression of H19 in calcified VSMCs, we induced VSMCs calcification with 10 mM beta-glycerophosphate. By qPCR and Western Blot analysis, we found that the expression of lncRNA H19, Runx2 and OSX were all highly increased in calcified VSMCs compared with normal VSMCs, while the expression of VSMCs differentiation markers, SM22-alpha and alpha-SMA, were significantly decreased. SiRNA study showed that knockdown of lncRNA H19 can decrease VSMCs calcification and Runx2 expression. We further validated that lncRNA H19 promoted VSMCs calcification via the p38 MAPK and ERK1/2 signal transduction pathways. As a conclusion, the present study showed that IncRNA H19/Runx2 axis promotes VSMCs transition via MAPK pathway. This finding not only reveal a novel function of lncRNA H19, but also provides a new opinion on the role of lncRNA H19 which participant in the Runx2 regulatory pathway in AC and can be a new indication for the diagnosis and treatment of AC at an early time.