- Meeting abstract
- Open Access
- Published:
Patients with unstable angina and myocardial infarction expose remote VSMC phenotype switch and alteration in the proliferation of smooth muscular cell in the aortic wall
Journal of Cardiothoracic Surgery volume 10, Article number: A238 (2015)
Background/Introduction
Vascular smooth muscular cell (VSMC) involve in vessel tone regulation and endothelial cell function. It is known and critical player in pathological conditions including atherosclerosis. VSMC is dynamic structure and response to different stimuli. MiRNAs molecules are important regulatory mechanism to promote/suppress VSMC proliferation and phenotype switch.
Aims/Objectives
Aim: We hypothesized that patients with acute myocardial infarction have altered VSMC transcriptome affecting cell phenotype and proliferation.
Method
Methods: Aortic wall tissue obtained during coronary artery bypass surgery underwent laser dissection of VSMC. Frozen aortic sections were stained with Arcturus LCM kit to identify cells of interest follow by cell collection and tRNA extraction. The transcriptome profile will be performed using Affymetrix GeneChip® Human Genome U133 Plus 2.0 Array. The differently expressed mRNA/miRNA data were validated on independent cohort of patients with RT-PCR method assay.
Results
Result: We identify nine miRNA differentially expressed in patients with acute myocardial infarction, with four of them related to VSMC proliferation and differentiation. The most prominent down regulated miRNA was known regulator of VSMC phenotype miR-143. Among up regulated miRNA, miR-486-5p and miR-29a-3p reported before as a potent regulator of VSMC function. Pairwise analysis with mRNA data from the same patients reveal reciprocal and statistically significant changes in the phenotype and proliferation related mRNA.
Discussion/Conclusion
Conclusion: In patients with acute myocardial infarction we observe remote phenotype and proliferation shift in the aortic wall VSMC. Switch of contractile phenotype and proliferation alteration might play compensatory role in patient with unstable plaque and myocardial infarction.
Author information
Authors and Affiliations
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made.
The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.
To view a copy of this licence, visit https://creativecommons.org/licenses/by/4.0/.
The Creative Commons Public Domain Dedication waiver (https://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
About this article
Cite this article
Woo, C.C., Zhiqun, T., Chan, Y.S. et al. Patients with unstable angina and myocardial infarction expose remote VSMC phenotype switch and alteration in the proliferation of smooth muscular cell in the aortic wall. J Cardiothorac Surg 10, A238 (2015). https://doi.org/10.1186/1749-8090-10-S1-A238
Published:
DOI: https://doi.org/10.1186/1749-8090-10-S1-A238
Keywords
- Acute Myocardial Infarction
- Aortic Wall
- Affymetrix GeneChip
- Endothelial Cell Function
- Phenotype Switch