Acute injury to the mouse carotid artery provokes a distinct healing response
Treatment of vascular stenosis with angioplasty results in acute vascular damage, which may lead to restenosis. Owing to the highly complex cellularity of blood vessels, the healing response following this damage is incompletely understood. To gain further insight into this process, scRNA-seq of mou...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-02-01
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| Series: | Frontiers in Physiology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2023.1125864/full |
| _version_ | 1811170470581501952 |
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| author | Timothy Warwick Timothy Warwick Giulia Karolin Buchmann Giulia Karolin Buchmann Beatrice Pflüger-Müller Beatrice Pflüger-Müller Manuela Spaeth Manuela Spaeth Christoph Schürmann Christoph Schürmann Wesley Abplanalp Wesley Abplanalp Lukas Tombor Lukas Tombor David John David John Andreas Weigert Martin Leo-Hansmann Stefanie Dimmeler Stefanie Dimmeler Ralf P. Brandes Ralf P. Brandes |
| author_facet | Timothy Warwick Timothy Warwick Giulia Karolin Buchmann Giulia Karolin Buchmann Beatrice Pflüger-Müller Beatrice Pflüger-Müller Manuela Spaeth Manuela Spaeth Christoph Schürmann Christoph Schürmann Wesley Abplanalp Wesley Abplanalp Lukas Tombor Lukas Tombor David John David John Andreas Weigert Martin Leo-Hansmann Stefanie Dimmeler Stefanie Dimmeler Ralf P. Brandes Ralf P. Brandes |
| author_sort | Timothy Warwick |
| collection | DOAJ |
| description | Treatment of vascular stenosis with angioplasty results in acute vascular damage, which may lead to restenosis. Owing to the highly complex cellularity of blood vessels, the healing response following this damage is incompletely understood. To gain further insight into this process, scRNA-seq of mouse carotid tissue after wire injury was performed. Stages of acute inflammation, resolution and remodeling were recapitulated in these data. To identify cell types which give rise to neointima, analyses focused on smooth muscle cell and fibroblast populations, and included data integration with scRNA-seq data from myocardial infarction and atherosclerosis datasets. Following carotid injury, a subpopulation of smooth muscle cells which also arises during atherosclerosis and myocardial infarction was identified. So-called stem cell/endothelial cell/monocyte (SEM) cells are candidates for repopulating injured vessels, and were amongst the most proliferative cell clusters following wire-injury of the carotid artery. Importantly, SEM cells exhibit specific transcriptional profiles which could be therapeutically targeted. SEM cell gene expression patterns could also be detected in bulk RNA-sequencing of neointimal tissue isolated from injured carotid vessels by laser capture microdissection. These data indicate that phenotypic plasticity of smooth muscle cells is highly important to the progression of lumen loss following acute carotid injury. Interference with SEM cell formation could be an innovative approach to combat development of restenosis. |
| first_indexed | 2024-04-10T16:57:17Z |
| format | Article |
| id | doaj.art-454a1536af07482ea7ac4e54de55b5f6 |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-04-10T16:57:17Z |
| publishDate | 2023-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Physiology |
| spelling | doaj.art-454a1536af07482ea7ac4e54de55b5f62023-02-07T04:36:30ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2023-02-011410.3389/fphys.2023.11258641125864Acute injury to the mouse carotid artery provokes a distinct healing responseTimothy Warwick0Timothy Warwick1Giulia Karolin Buchmann2Giulia Karolin Buchmann3Beatrice Pflüger-Müller4Beatrice Pflüger-Müller5Manuela Spaeth6Manuela Spaeth7Christoph Schürmann8Christoph Schürmann9Wesley Abplanalp10Wesley Abplanalp11Lukas Tombor12Lukas Tombor13David John14David John15Andreas Weigert16Martin Leo-Hansmann17Stefanie Dimmeler18Stefanie Dimmeler19Ralf P. Brandes20Ralf P. Brandes21Institute for Cardiovascular Physiology, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute for Cardiovascular Physiology, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute for Cardiovascular Physiology, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute for Cardiovascular Physiology, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute for Cardiovascular Physiology, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute of Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute of Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute of Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, GermanyInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt am Main, GermanyDepartment of Pathology, University Hospital Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyInstitute of Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, GermanyInstitute for Cardiovascular Physiology, Goethe University Frankfurt, Frankfurt am Main, GermanyGerman Center for Cardiovascular Research (DZHK), Partner site Rhein Main, Frankfurt am Main, GermanyTreatment of vascular stenosis with angioplasty results in acute vascular damage, which may lead to restenosis. Owing to the highly complex cellularity of blood vessels, the healing response following this damage is incompletely understood. To gain further insight into this process, scRNA-seq of mouse carotid tissue after wire injury was performed. Stages of acute inflammation, resolution and remodeling were recapitulated in these data. To identify cell types which give rise to neointima, analyses focused on smooth muscle cell and fibroblast populations, and included data integration with scRNA-seq data from myocardial infarction and atherosclerosis datasets. Following carotid injury, a subpopulation of smooth muscle cells which also arises during atherosclerosis and myocardial infarction was identified. So-called stem cell/endothelial cell/monocyte (SEM) cells are candidates for repopulating injured vessels, and were amongst the most proliferative cell clusters following wire-injury of the carotid artery. Importantly, SEM cells exhibit specific transcriptional profiles which could be therapeutically targeted. SEM cell gene expression patterns could also be detected in bulk RNA-sequencing of neointimal tissue isolated from injured carotid vessels by laser capture microdissection. These data indicate that phenotypic plasticity of smooth muscle cells is highly important to the progression of lumen loss following acute carotid injury. Interference with SEM cell formation could be an innovative approach to combat development of restenosis.https://www.frontiersin.org/articles/10.3389/fphys.2023.1125864/fullsmooth muscle cellsphenotypic switchingvascular injurysingle-cellhealingneointima |
| spellingShingle | Timothy Warwick Timothy Warwick Giulia Karolin Buchmann Giulia Karolin Buchmann Beatrice Pflüger-Müller Beatrice Pflüger-Müller Manuela Spaeth Manuela Spaeth Christoph Schürmann Christoph Schürmann Wesley Abplanalp Wesley Abplanalp Lukas Tombor Lukas Tombor David John David John Andreas Weigert Martin Leo-Hansmann Stefanie Dimmeler Stefanie Dimmeler Ralf P. Brandes Ralf P. Brandes Acute injury to the mouse carotid artery provokes a distinct healing response Frontiers in Physiology smooth muscle cells phenotypic switching vascular injury single-cell healing neointima |
| title | Acute injury to the mouse carotid artery provokes a distinct healing response |
| title_full | Acute injury to the mouse carotid artery provokes a distinct healing response |
| title_fullStr | Acute injury to the mouse carotid artery provokes a distinct healing response |
| title_full_unstemmed | Acute injury to the mouse carotid artery provokes a distinct healing response |
| title_short | Acute injury to the mouse carotid artery provokes a distinct healing response |
| title_sort | acute injury to the mouse carotid artery provokes a distinct healing response |
| topic | smooth muscle cells phenotypic switching vascular injury single-cell healing neointima |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2023.1125864/full |
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