Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Abstract

Background Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. Methods The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1. Results The levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL. Conclusion Overexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis.

LncRNA HOTAIR Inhibits miR-19a-3p to Alleviate Foam Cell Formation and Inflammatory Response in Atherosclerosis

“…Mounting evidence suggests that lncRNA dysregulation is closely associated with human diseases, including atherosclerosis, where they play significant roles. For instance, the lncRNAs H19, TUG1, and Neat1 are upregulated in atherosclerosis and contribute to vascular smooth muscle cell (VSMC) proliferation while inhibiting apoptosis On the other hand, the downregulation of UCA1, MEG3, lincRNA-p21, and GASL1 in atherosclerosis leads to suppressed VSMC proliferation and inflammation [8,[38][39][40]. In our previous research, we observed increased expression of miR-19a-3p in the serum and atherosclerotic plaques of patients with atherosclerosis.…”

Omega-3 fatty acids and individual variability in plasma triglyceride response: A mini-review

“…Furthermore, the concentration of 11 circulating miRNAs was altered during the intervention, including miR-106a, which correlated with the change in plasma EPA levels and TG levels [ 50 ]. miR-106a has recently been suggested to play a role in the development of atherosclerosis [ 65 ]. Moreover, miR-122 and miR-33 are important regulators of lipid metabolism, controlling the expression of genes in fatty acid and cholesterol metabolism, including fatty acid synthase ( FAS ), sterol regulatory element binding transcription factor 1 ( SREBF1 ), ATP binding cassette subfamily A member 1 ( ABCA1 ), ATP binding cassette subfamily G member 1 ( ABCG1 ) and carnitine palmitoyltransferase 1A ( CPT1A ) [ 66 , 67 ].…”