The upregulation of lamin A/C as a compensatory mechanism during tight junction disruption in renal tubular cells mediated by calcium oxalate crystals.
COM
Kidney stone
LMNA
Protein-protein interaction
Tight junction
Transepithelial resistance
ZO-1
Journal
Current research in toxicology
ISSN: 2666-027X
Titre abrégé: Curr Res Toxicol
Pays: Netherlands
ID NLM: 101771915
Informations de publication
Date de publication:
2024
2024
Historique:
received:
16
07
2023
revised:
12
11
2023
accepted:
13
12
2023
medline:
9
1
2024
pubmed:
9
1
2024
entrez:
9
1
2024
Statut:
epublish
Résumé
Calcium oxalate monohydrate (COM), the most important crystal causing kidney stone disease, upregulates lamin A/C but downregulates zonula occludens-1 (ZO-1) in renal tubular cells. While roles for F-actin and α-tubulin and their association with ZO-1 are known to regulate COM-mediated tight junction (TJ) disruption, roles of lamin A/C and its interplay with ZO-1 in COM kidney stone model remain unclear and are thus the objectives of this study. Lamin A/C was knocked down in MDCK cells by silencing RNA specific for
Identifiants
pubmed: 38193033
doi: 10.1016/j.crtox.2023.100145
pii: S2666-027X(23)00043-9
pmc: PMC10772403
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100145Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.