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Copyright (c) 2023 Junbo Feng, Yuntao Hu, Peng Peng, Juntao Li, Shenglin Ge
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.PKD1 participates in the processing of aortic dissection via regulating vascular smooth muscle cell contraction and MAPK signaling
Corresponding Author(s) : Junbo Feng
Cellular and Molecular Biology,
Vol. 69 No. 10: Issue 10
Abstract
Aortic Dissection (AD) is a cardiovascular emergency with high mortality, of which one feature is the phenotypic switch of vascular smooth muscle cells (VSMCs). Transient Receptor Potential Channel Interacting (PKD1) has been regarded as one regulator as well as one biomarker for AD. However, multiple candidate pathways were reported though which PKD1 regulates AD in previous study, a comprehensive insight is still absent. In this study, we compared the AD and normal samples in transcriptome scale, and detected 717 PKD1-related differential expressed genes, which enriched in mitogen-activated protein kinase (MAPK) signal transduction (AD tissue preference) and VSMC contraction pathway (normal tissue preference). Furthermore, we also found two important functional hub genes in PKD1 regulation, JUN and ACTN2, and established a carnal-miRNA-mRNA network. Our study demonstrated the co-regulation of muscle development and signal transduction in AD’s progression, and also provided the genetic basis for the following mechanism research with AD.
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