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Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat
The pathology of cerebrovascular disorders, such as hypertension, is associated with genetic changes and dysfunction of basilar artery smooth muscle cells (BASMCs). Long-term high-salt diets have been associated with the development of hypertension. However, the molecular mechanisms underlying salt-...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PeerJ Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7566752/ https://www.ncbi.nlm.nih.gov/pubmed/33083107 http://dx.doi.org/10.7717/peerj.9849 |
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author | Huang, Junhao Zhang, Lesha Fang, Yang Jiang, Wan Du, Juan Zhu, Jinhang Hu, Min Shen, Bing |
author_facet | Huang, Junhao Zhang, Lesha Fang, Yang Jiang, Wan Du, Juan Zhu, Jinhang Hu, Min Shen, Bing |
author_sort | Huang, Junhao |
collection | PubMed |
description | The pathology of cerebrovascular disorders, such as hypertension, is associated with genetic changes and dysfunction of basilar artery smooth muscle cells (BASMCs). Long-term high-salt diets have been associated with the development of hypertension. However, the molecular mechanisms underlying salt-sensitive hypertension-induced BASMC modifications have not been well defined, especially at the level of variations in gene transcription. Here, we utilized high-throughput sequencing and subsequent signaling pathway analyses to find a two–fold change or greater upregulated expression of 203 transcripts and downregulated expression of 165 transcripts in BASMCs derived from rats fed a high-salt diet compared with those from control rats. These differentially expressed transcripts were enriched in pathways involved in cellular, morphological, and structural plasticity, autophagy, and endocrine regulation. These transcripts changes in the BASMCs derived from high-salt intake–induced hypertensive rats may provide critical information about multiple cellular processes and biological functions that occur during the development of cerebrovascular disorders and provide potential new targets to help control or block the development of hypertension. |
format | Online Article Text |
id | pubmed-7566752 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | PeerJ Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-75667522020-10-19 Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat Huang, Junhao Zhang, Lesha Fang, Yang Jiang, Wan Du, Juan Zhu, Jinhang Hu, Min Shen, Bing PeerJ Bioinformatics The pathology of cerebrovascular disorders, such as hypertension, is associated with genetic changes and dysfunction of basilar artery smooth muscle cells (BASMCs). Long-term high-salt diets have been associated with the development of hypertension. However, the molecular mechanisms underlying salt-sensitive hypertension-induced BASMC modifications have not been well defined, especially at the level of variations in gene transcription. Here, we utilized high-throughput sequencing and subsequent signaling pathway analyses to find a two–fold change or greater upregulated expression of 203 transcripts and downregulated expression of 165 transcripts in BASMCs derived from rats fed a high-salt diet compared with those from control rats. These differentially expressed transcripts were enriched in pathways involved in cellular, morphological, and structural plasticity, autophagy, and endocrine regulation. These transcripts changes in the BASMCs derived from high-salt intake–induced hypertensive rats may provide critical information about multiple cellular processes and biological functions that occur during the development of cerebrovascular disorders and provide potential new targets to help control or block the development of hypertension. PeerJ Inc. 2020-10-13 /pmc/articles/PMC7566752/ /pubmed/33083107 http://dx.doi.org/10.7717/peerj.9849 Text en ©2020 Huang et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited. |
spellingShingle | Bioinformatics Huang, Junhao Zhang, Lesha Fang, Yang Jiang, Wan Du, Juan Zhu, Jinhang Hu, Min Shen, Bing Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
title | Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
title_full | Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
title_fullStr | Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
title_full_unstemmed | Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
title_short | Differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
title_sort | differentially expressed transcripts and associated protein pathways in basilar artery smooth muscle cells of the high-salt intake–induced hypertensive rat |
topic | Bioinformatics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7566752/ https://www.ncbi.nlm.nih.gov/pubmed/33083107 http://dx.doi.org/10.7717/peerj.9849 |
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