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LncRNA MALAT1 suppresses monocyte-endothelial cell interactions by targeting miR-30b-5p and enhancing ATG5-mediated
Xiaodong Gu1,2,3, Jingyuan Hou1,2,3, Jiawei Rao4
1Meizhou Clinical Institute, Shantou University Medical College, Meizhou, 514000, China.
Background:
Monocyte-endothelial cell (EC) interactions are one of the earliest events in the development of atherosclerosis and play a crucial role in atherosclerotic plaque formation. Although attempts have been made to modulate this interaction, the underlying molecular signalling mechanisms remain unclear. This study aimed to investigate the role of long non-coding RNA MALAT1 in monocyte-EC interactions.
Methods:
The expression of MALAT1, ICAM-1, VCAM-1, P-selectin, CCL2 and CXCL1 was evaluated in ApoE-/- mouse aortic tissues and inflamed human umbilical vein endothelial cells (HUVECs). The regulatory impact of MALAT1 on cell adhesion molecules, monocyte-EC adhesion, and autophagy was assessed. The interactions between MALAT1 and microRNAs (miRNAs) were evaluated using dual-luciferase reporter and RNA pull-down assays.
Results:
MALAT1 expression decreased in ApoE-/- mouse aortic tissues and inflammatory HUVECs. MALAT1 overexpression suppressed the expression of ICAM-1, VCAM-1 and CXCL1, and reduced the migration and adhesion of monocytes to ECs. Inhibition of MALAT1 promoted cell adhesion molecule expression and monocyte-EC interactions. Mechanistically, MALAT1 binds directly to miR-30b-5p and decreases its effective expression by functioning as an endogenous sponge, thereby increasing the expression of autophagy-related gene 5 (ATG5) and stimulates endothelial autophagy.
Conclusions:
Our findings suggest that MALAT1 suppresses monocyte-EC interactions by targeting miR-30b-5p and enhancing ATG5-mediated endothelial autophagy. These data imply that MALAT1 may play a protective role at the early stages of the atherosclerotic process.
Insights
Long non-coding RNA MALAT1 suppresses monocyte-endothelial cell interactions by targeting miR-30b-5p and enhancing autophagy. This suggests MALAT1 may protect against early atherosclerosis development.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- RNA Biology
Background:
- Monocyte-endothelial cell (EC) interactions are pivotal in early atherosclerosis.
- Molecular mechanisms regulating these interactions remain incompletely understood.
- Investigating long non-coding RNAs (lncRNAs) offers potential insights.
Purpose of the Study:
- To elucidate the role of lncRNA MALAT1 in monocyte-EC interactions.
- To identify molecular pathways modulated by MALAT1 in this context.
Main Methods:
- Assessed expression of MALAT1 and adhesion molecules in ApoE-/- mouse aortas and inflamed HUVECs.
- Evaluated MALAT1's impact on monocyte-EC adhesion and autophagy.
- Investigated MALAT1-microRNA interactions using luciferase and pull-down assays.
Main Results:
- MALAT1 expression was reduced in atherosclerotic models.
- MALAT1 overexpression inhibited adhesion molecules and monocyte adhesion to ECs.
- MALAT1 acts as a sponge for miR-30b-5p, upregulating ATG5 and promoting endothelial autophagy.
Conclusions:
- MALAT1 suppresses monocyte-EC interactions via miR-30b-5p and ATG5-mediated autophagy.
- MALAT1 demonstrates a protective role in early atherosclerosis.
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