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Published on: August 3, 2018
Transcriptomics of angiotensin II-induced long noncoding and coding RNAs in endothelial cells
Shuhan Bu1, Hien C Nguyen1,2, David C R Michels1
1Department of Medical Biophysics.
This study reveals novel long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) affected by Angiotensin II (Ang II) in human endothelial cells. These findings offer new insights into Ang II-induced endothelial dysfunction and cardiovascular diseases.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genomics
Background:
- Endothelial dysfunction induced by Angiotensin II (Ang II) is a key factor in cardiovascular diseases.
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their role in cardiovascular pathobiology.
- The impact of Ang II on lncRNA and coding RNA expression in endothelial cells remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression profiles of lncRNAs and coding RNAs in human endothelial cells upon Ang II treatment.
- To identify novel differentially expressed lncRNAs and mRNAs in response to Ang II.
- To explore the potential roles of these altered RNAs in Ang II-induced endothelial dysfunction.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were cultured and exposed to Ang II.
- Global expression profiling of lncRNAs and mRNAs was performed using microarray technology.
- Bioinformatic analysis was employed to identify differentially expressed genes and their functional pathways.
Main Results:
- Ang II treatment significantly altered the expression of numerous lncRNAs and mRNAs in HUVECs.
- Specific lncRNAs, such as RP11-354P11.2 (upregulated) and RP11-360F5.1 (downregulated), were identified.
- Functional enrichment analysis indicated involvement in pathways like nucleotide excision repair and ECM-receptor interaction.
Conclusions:
- This study provides the first comprehensive profile of Ang II-induced lncRNA and mRNA changes in human endothelial cells.
- The identified differentially expressed RNAs represent potential novel targets for understanding and treating Ang II-related endothelial dysfunction.
- These findings significantly expand the repertoire of candidate genes implicated in cardiovascular diseases.
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