Key result
RNCR3 knockdown accelerated the development of atherosclerosis, aggravated hypercholesterolemia, and decreased endothelial and vascular smooth muscle cell proliferation in vivo and in vitro.
Why the study?
Does RNCR3 knockdown accelerate atherosclerosis development and vascular dysfunction in ApoE-/- mice and cultured human vascular cells?
Does RNCR3 knockdown accelerate atherosclerosis development and vascular dysfunction in ApoE-/- mice and cultured human vascular cells?
p-value: p=<0.05
RNCR3 has an atheroprotective role by regulating endothelial and vascular smooth muscle cell function via a ceRNA network involving KLF2 and miR-185-5p.
RNCR3 may be atheroprotective in ApoE-/- mice; leaves open its therapeutic relevance in human atherosclerosis pending clinical studies.
Atherosclerosis is one of the most common vascular disorders. Endothelial cell (EC) dysfunction and vascular smooth muscle cell (VSMC) proliferation contributes to the development of atherosclerosis. Long non-coding RNAs (lncRNAs) have been implicated in several biological processes and human diseases. Here we show that lncRNA-RNCR3 is expressed in ECs and VSMCs. RNCR3 expression is significantly upregulated in mouse and human aortic atherosclerotic lesions, and cultured ECs and VSMCs upon ox-LDL treatment in vitro. RNCR3 knockdown accelerates the development of atherosclerosis, aggravates hypercholesterolemia and inflammatory factor releases, and decreases EC and VSMC proliferation in vivo. RNCR3 knockdown also reduces the proliferation and migration, and accelerates apoptosis development of EC and VSMC in vitro. RNCR3 acts as a ceRNA, and forms a feedback loop with Kruppel-like factor 2 and miR-185-5p to regulate cell function. This study reveals that RNCR3 has an atheroprotective role in atherosclerosis, and its intervention is a promising strategy for treating atherosclerosis-related vascular dysfunction.
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Shan et al. (2016) studied Atherosclerosis. RNCR3 knockdown vs. Scrambled shRNA/siRNA or PBS was evaluated on Atherosclerotic lesion area and cellular function (proliferation/apoptosis) (p=<0.05). RNCR3 knockdown accelerated the development of atherosclerosis, aggravated hypercholesterolemia, and decreased endothelial and vascular smooth muscle cell proliferation in vivo and in vitro.
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