Abstract | OBJECTIVE: METHODS AND RESULTS: Using cultured VSMCs, we found that Ang II increased cellular OPN protein expression 4 h after treatment by 420 ± 54% (p < 0.03) in a translation dependent manner. Sequence analysis revealed a putative binding site for mir181a and raised the possibility that miR181a is a potential regulatory mechanism for OPN expression. We demonstrated that Ang II decreased miR181a expression by 52 ± 7% (p < 0 .0001) and overexpressing miR181a inhibited Ang II induced increases in OPN protein expression by 69 ± 9% (p < 0.05). Furthermore, we demonstrated that miR181a is functionally important in that overexpression of miR181a inhibited VSMCs adhesion to collagen in response to Ang II as compared to controls by 36 ± 4%. (p < 0.05) CONCLUSIONS: These results demonstrate that miR181a regulates OPN expression and that altering miR181a expression may be a novel therapeutic approach to modulate OPN protein expression.
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Authors | Ebony Washington Remus, Alicia N Lyle, Daiana Weiss, Natalia Landàzuri, Martina Weber, Charles Searles, W Robert Taylor |
Journal | Atherosclerosis
(Atherosclerosis)
Vol. 228
Issue 1
Pg. 168-74
(May 2013)
ISSN: 1879-1484 [Electronic] Ireland |
PMID | 23466073
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Copyright | Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- MIRN181 microRNA, rat
- MicroRNAs
- RNA, Messenger
- Spp1 protein, rat
- Vasoconstrictor Agents
- Osteopontin
- Angiotensin II
|
Topics |
- Angiotensin II
(pharmacology)
- Animals
- Aorta
(cytology)
- Cells, Cultured
- Gene Expression
(drug effects, physiology)
- MicroRNAs
(genetics, pharmacology)
- Muscle, Smooth, Vascular
(cytology, physiology)
- Osteopontin
(genetics)
- RNA, Messenger
(metabolism)
- Rats
- Transcription, Genetic
(drug effects, physiology)
- Vasoconstrictor Agents
(pharmacology)
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