Research Paper Volume 12, Issue 15 pp 15603—15623
Transcriptome analysis of mouse aortae reveals multiple novel pathways regulated by aging
- 1 Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA
- 2 Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA
- 3 School of Public Health, University at Albany, Albany, NY 12222, USA
Received: March 28, 2020 Accepted: June 22, 2020 Published: August 15, 2020https://doi.org/10.18632/aging.103652
How to Cite
Copyright © 2020 Gao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Vascular aging has been documented as a vital process leading to arterial dysfunction and age-related cardiovascular and cerebrovascular diseases. However, our understanding of the molecular underpinnings of age-related phenotypes in the vascular system is incomplete. Here we performed bulk RNA sequencing in young and old mouse aortae to elucidate age-associated changes in the transcriptome. Results showed that the majority of upregulated pathways in aged aortae relate to immune response, including inflammation activation, apoptotic clearance, and phagocytosis. The top downregulated pathway in aged aortae was extracellular matrix organization. Additionally, protein folding control and stress response pathways were downregulated in the aged vessels, with an array of downregulated genes encoding heat shock proteins (HSPs). We also found that circadian core clock genes were differentially expressed in young versus old aortae. Finally, transcriptome analysis combined with protein expression examination and smooth muscle cell (SMC) lineage tracing revealed that SMCs in aged aortae retained the differentiated phenotype, with an insignificant decrease in SMC marker gene expression. Our results therefore unveiled critical pathways regulated by arterial aging in mice, which will provide important insight into strategies to defy vascular aging and age-associated vascular diseases.