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Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation
The heart is one of the major organs affected by microwave radiation, and these effects have been extensively studied. Previous studies have shown that microwave-radiation-induced heart injury might be related to the abnormal expression and distribution of Cx43. In order to make the research model c...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10454302/ https://www.ncbi.nlm.nih.gov/pubmed/37628714 http://dx.doi.org/10.3390/ijms241612533 |
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author | Yin, Yue Xu, Xinping Li, Dayan Yao, Binwei Wang, Haoyu Zhao, Li Wang, Hui Dong, Ji Zhang, Jing Peng, Ruiyun |
author_facet | Yin, Yue Xu, Xinping Li, Dayan Yao, Binwei Wang, Haoyu Zhao, Li Wang, Hui Dong, Ji Zhang, Jing Peng, Ruiyun |
author_sort | Yin, Yue |
collection | PubMed |
description | The heart is one of the major organs affected by microwave radiation, and these effects have been extensively studied. Previous studies have shown that microwave-radiation-induced heart injury might be related to the abnormal expression and distribution of Cx43. In order to make the research model closer to humans, we used iPSC-CMs as the cell injury model to investigate the biological effect and mechanism of iPSC-CM injury after microwave radiation. To model the damage, iPSC-CMs were separated into four groups and exposed to single or composite S-band (2.856 GHz) and X-band (9.375 GHz) microwave radiation sources with an average power density of 30 mW/cm(2). After that, FCM was used to detect cell activity, and ELISA was used to detect the contents of myocardial enzymes and injury markers in the culture medium, and it was discovered that cell activity decreased and the contents increased after radiation. TEM and SEM showed that the ultrastructure of the cell membrane, mitochondria, and ID was damaged. Mitochondrial function was aberrant, and glycolytic capacity decreased after exposure. The electrical conduction function of iPSC-CM was abnormal; the conduction velocity was decreased, and the pulsation amplitude was reduced. Wb, qRT-PCR, and IF detections showed that the expression of Cx43 was decreased and the distribution of Cx43 at the gap junction was disordered. Single or composite exposure to S- and X-band microwave radiation caused damage to the structure and function of iPSC-CMs, primarily affecting the cell membrane, mitochondria, and ID. The composite exposure group was more severely harmed than the single exposure group. These abnormalities in structure and function were related to the decreased expression and disordered distribution of Cx43. |
format | Online Article Text |
id | pubmed-10454302 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-104543022023-08-26 Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation Yin, Yue Xu, Xinping Li, Dayan Yao, Binwei Wang, Haoyu Zhao, Li Wang, Hui Dong, Ji Zhang, Jing Peng, Ruiyun Int J Mol Sci Article The heart is one of the major organs affected by microwave radiation, and these effects have been extensively studied. Previous studies have shown that microwave-radiation-induced heart injury might be related to the abnormal expression and distribution of Cx43. In order to make the research model closer to humans, we used iPSC-CMs as the cell injury model to investigate the biological effect and mechanism of iPSC-CM injury after microwave radiation. To model the damage, iPSC-CMs were separated into four groups and exposed to single or composite S-band (2.856 GHz) and X-band (9.375 GHz) microwave radiation sources with an average power density of 30 mW/cm(2). After that, FCM was used to detect cell activity, and ELISA was used to detect the contents of myocardial enzymes and injury markers in the culture medium, and it was discovered that cell activity decreased and the contents increased after radiation. TEM and SEM showed that the ultrastructure of the cell membrane, mitochondria, and ID was damaged. Mitochondrial function was aberrant, and glycolytic capacity decreased after exposure. The electrical conduction function of iPSC-CM was abnormal; the conduction velocity was decreased, and the pulsation amplitude was reduced. Wb, qRT-PCR, and IF detections showed that the expression of Cx43 was decreased and the distribution of Cx43 at the gap junction was disordered. Single or composite exposure to S- and X-band microwave radiation caused damage to the structure and function of iPSC-CMs, primarily affecting the cell membrane, mitochondria, and ID. The composite exposure group was more severely harmed than the single exposure group. These abnormalities in structure and function were related to the decreased expression and disordered distribution of Cx43. MDPI 2023-08-08 /pmc/articles/PMC10454302/ /pubmed/37628714 http://dx.doi.org/10.3390/ijms241612533 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Yin, Yue Xu, Xinping Li, Dayan Yao, Binwei Wang, Haoyu Zhao, Li Wang, Hui Dong, Ji Zhang, Jing Peng, Ruiyun Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation |
title | Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation |
title_full | Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation |
title_fullStr | Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation |
title_full_unstemmed | Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation |
title_short | Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation |
title_sort | role of cx43 in ipsc-cm damage induced by microwave radiation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10454302/ https://www.ncbi.nlm.nih.gov/pubmed/37628714 http://dx.doi.org/10.3390/ijms241612533 |
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