Exploring molecular profiles of calcification in aortic vascular smooth muscle cells and aortic valvular interstitial cells.
Aortic valve interstitial cell
Aortic vascular smooth muscle cell
Calcification
Heart valve
Vasculature
Journal
Journal of molecular and cellular cardiology
ISSN: 1095-8584
Titre abrégé: J Mol Cell Cardiol
Pays: England
ID NLM: 0262322
Informations de publication
Date de publication:
Oct 2023
Oct 2023
Historique:
received:
07
02
2023
revised:
26
07
2023
accepted:
08
08
2023
pmc-release:
01
10
2024
medline:
3
11
2023
pubmed:
15
8
2023
entrez:
14
8
2023
Statut:
ppublish
Résumé
Cardiovascular calcification can occur in vascular and valvular structures and is commonly associated with calcium deposition and tissue mineralization leading to stiffness and dysfunction. Patients with chronic kidney disease and associated hyperphosphatemia have an elevated risk for coronary artery calcification (CAC) and calcific aortic valve disease (CAVD). However, there is mounting evidence to suggest that the susceptibility and pathobiology of calcification in these two cardiovascular structures may be different, yet clinically they are similarly treated. To better understand diversity in molecular and cellular processes that underlie hyperphosphatemia-induced calcification in vascular and valvular structures, we exposed aortic vascular smooth muscle cells (AVSMCs) and aortic valve interstitial cells (AVICs) to high (2.5 mM) phosphate (Ph) conditions in vitro, and examined cell-specific responses. To further identify hyperphosphatemic-specific responses, parallel studies were performed using osteogenic media (OM) as an alternative calcific stimulus. Consistent with clinical observations made by others, we show that AVSMCs are more susceptible to calcification than AVICs. In addition, bulk RNA-sequencing reveals that AVSMCs and AVICs activate robust ossification-programs in response to high phosphate or OM treatments, however, the signaling pathways, cellular processes and osteogenic-associated markers involved are cell- and treatment-specific. For example, compared to VSMCs, VIC-mediated calcification involves biological processes related to osteo-chondro differentiation and down regulation of 'actin cytoskeleton'-related genes, that are not observed in VSMCs. Furthermore, hyperphosphatemic-induced calcification in AVICs and AVSMCs is independent of P13K signaling, which plays a role in OM-treated cells. Together, this study provides a wealth of information suggesting that the pathogenesis of cardiovascular calcifications is significantly more diverse than previously appreciated.
Identifiants
pubmed: 37579636
pii: S0022-2828(23)00126-8
doi: 10.1016/j.yjmcc.2023.08.001
pmc: PMC10592135
mid: NIHMS1924428
pii:
doi:
Substances chimiques
Phosphates
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-13Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL142685
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL159802
Pays : United States
Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest None.
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