Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations

Abstract Thoracic aortopathy is influenced by angiotensin II (AngII) and exhibits regional heterogeneity with the ascending aorta being particularly susceptible. In this region, smooth muscle cells (SMCs) and selected fibroblasts originate from the second heart field (SHF) and cardiac neural crest (...

Full description

Saved in:
Bibliographic Details
Main Authors: Sohei Ito, David B. Graf, Yuriko Katsumata, Jessica J. Moorleghen, Chen Zhang, Yanming Li, Scott A. LeMaire, Ying H. Shen, Hong S. Lu, Alan Daugherty, Hisashi Sawada
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Scientific Reports
Subjects:
Online Access:https://doi.org/10.1038/s41598-025-99862-4
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849726102566600704
author Sohei Ito
David B. Graf
Yuriko Katsumata
Jessica J. Moorleghen
Chen Zhang
Yanming Li
Scott A. LeMaire
Ying H. Shen
Hong S. Lu
Alan Daugherty
Hisashi Sawada
author_facet Sohei Ito
David B. Graf
Yuriko Katsumata
Jessica J. Moorleghen
Chen Zhang
Yanming Li
Scott A. LeMaire
Ying H. Shen
Hong S. Lu
Alan Daugherty
Hisashi Sawada
author_sort Sohei Ito
collection DOAJ
description Abstract Thoracic aortopathy is influenced by angiotensin II (AngII) and exhibits regional heterogeneity with the ascending aorta being particularly susceptible. In this region, smooth muscle cells (SMCs) and selected fibroblasts originate from the second heart field (SHF) and cardiac neural crest (CNC). While our previous study revealed a critical role of SHF-derived cells in AngII-mediated aortopathy, the contribution of CNC-derived cells remains unclear. To investigate lineage-specific responses to AngII, Mef2c-Cre R26RmT/mG mice were infused with AngII. Ascending aortas were harvested at baseline or after 3 days of infusion, representing the prepathological phase. Cells were sorted based on their embryonic origins and single-cell RNA sequencing was performed. Transcriptomic analysis revealed significant changes in both SHF- and nSHF-derived SMCs following short-term AngII infusion, although differences between the origins were modest. Similarly, fibroblast transcriptomes exhibited notable changes, yet lineage-specific differences remained modest, except for a newly identified fibroblast subpopulation where extracellular matrix-related genes such as Eln and Col3a1 were downregulated in SHF-derived fibroblasts compared to nSHF-derived fibroblasts. These findings suggest that while fibroblasts in the new subcluster exhibit lineage-specific extracellular matrix-related differences, overall transcriptomic variations between SHF- and nSHF-derived cells in response to AngII remain modest during the prepathological phase of AngII-induced thoracic aortopathy.
format Article
id doaj-art-358e16b67b634e53a07a24072afc2c53
institution DOAJ
issn 2045-2322
language English
publishDate 2025-05-01
publisher Nature Portfolio
record_format Article
series Scientific Reports
spelling doaj-art-358e16b67b634e53a07a24072afc2c532025-08-20T03:10:18ZengNature PortfolioScientific Reports2045-23222025-05-0115111210.1038/s41598-025-99862-4Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterationsSohei Ito0David B. Graf1Yuriko Katsumata2Jessica J. Moorleghen3Chen Zhang4Yanming Li5Scott A. LeMaire6Ying H. Shen7Hong S. Lu8Alan Daugherty9Hisashi Sawada10Saha Cardiovascular Research Center, College of Medicine, University of KentuckySaha Cardiovascular Research Center, College of Medicine, University of KentuckyDepartment of Biostatistics, College of Public Health, College of Medicine, University of KentuckySaha Cardiovascular Research Center, College of Medicine, University of KentuckyDivision of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of MedicineDivision of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of MedicineDivision of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of MedicineDivision of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of MedicineSaha Cardiovascular Research Center, College of Medicine, University of KentuckySaha Cardiovascular Research Center, College of Medicine, University of KentuckySaha Cardiovascular Research Center, College of Medicine, University of KentuckyAbstract Thoracic aortopathy is influenced by angiotensin II (AngII) and exhibits regional heterogeneity with the ascending aorta being particularly susceptible. In this region, smooth muscle cells (SMCs) and selected fibroblasts originate from the second heart field (SHF) and cardiac neural crest (CNC). While our previous study revealed a critical role of SHF-derived cells in AngII-mediated aortopathy, the contribution of CNC-derived cells remains unclear. To investigate lineage-specific responses to AngII, Mef2c-Cre R26RmT/mG mice were infused with AngII. Ascending aortas were harvested at baseline or after 3 days of infusion, representing the prepathological phase. Cells were sorted based on their embryonic origins and single-cell RNA sequencing was performed. Transcriptomic analysis revealed significant changes in both SHF- and nSHF-derived SMCs following short-term AngII infusion, although differences between the origins were modest. Similarly, fibroblast transcriptomes exhibited notable changes, yet lineage-specific differences remained modest, except for a newly identified fibroblast subpopulation where extracellular matrix-related genes such as Eln and Col3a1 were downregulated in SHF-derived fibroblasts compared to nSHF-derived fibroblasts. These findings suggest that while fibroblasts in the new subcluster exhibit lineage-specific extracellular matrix-related differences, overall transcriptomic variations between SHF- and nSHF-derived cells in response to AngII remain modest during the prepathological phase of AngII-induced thoracic aortopathy.https://doi.org/10.1038/s41598-025-99862-4AortopathyAneurysmDissectionAngiotensinSmooth muscle cellsFibroblasts
spellingShingle Sohei Ito
David B. Graf
Yuriko Katsumata
Jessica J. Moorleghen
Chen Zhang
Yanming Li
Scott A. LeMaire
Ying H. Shen
Hong S. Lu
Alan Daugherty
Hisashi Sawada
Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations
Scientific Reports
Aortopathy
Aneurysm
Dissection
Angiotensin
Smooth muscle cells
Fibroblasts
title Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations
title_full Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations
title_fullStr Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations
title_full_unstemmed Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations
title_short Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations
title_sort smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin ii driven transcriptional alterations
topic Aortopathy
Aneurysm
Dissection
Angiotensin
Smooth muscle cells
Fibroblasts
url https://doi.org/10.1038/s41598-025-99862-4
work_keys_str_mv AT soheiito smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT davidbgraf smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT yurikokatsumata smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT jessicajmoorleghen smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT chenzhang smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT yanmingli smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT scottalemaire smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT yinghshen smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT hongslu smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT alandaugherty smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations
AT hisashisawada smoothmusclecellsandfibroblastsintheascendingaortaexhibitminordifferencesbetweenembryonicoriginsinangiotensiniidriventranscriptionalalterations