Aims:We aimed to detected the biological function of LncRNA MALAT1 in regulating macrophage-related autophagy.
Atherosclerosis is the mainly cause of cardiovascular and cerebrovascular diseases, which lead to the second cause of death worldwide. In advanced atherosclerotic plaque, macrophage apoptosis coupled with inflammatory cytokines secretion promotes the formation of necrotic cores.
To demonstrate the MALAT1-related autophagy and find related signaling pathway.
We utilized ox-LDL to incubate THP-1-derived macrophages in order to establish the foam cell model in vitro. RT-qPCR and western blot analyses confirmed the increasing expression level of MALAT1 and autophagy-related protein LC-3, Beclin-1. Si-RNAs study showed the significant decrease in autophagy activity and increase in apoptotic rate when knocking down MALAT1. Further study demonstrated that MALAT1 inhibited the expression of MAPK and NF-κB (p65) by up-regulating SIRT1.
Here we demonstrated that the long non-coding RNA MALAT1, which has attracted increasingly attention by its potent function on gene transcription modulation, is also indispensable for maintaining oxidized low density lipoproteins (ox-LDL)-induced autophagy in macrophage. Besides, we also proved that MALAT1 exerted its protective function by activating SIRT1, which subsequently inhibit the MAPK and NF-κB signaling pathway.
LncRNA MALAT1 Enhances Ox-LDL-induced Autophagy via the SIRT1/MAPK/NF-κB Pathway in Macrophages.