Long non-coding RNA lnc-CHAF1B-3 promotes renal interstitial fibrosis by regulating EMT-related genes in renal proximal tubular cells.
IgA nephropathy
MT: Non-coding RNAs
epithelial-to-mesenchymal transition
lnc-CHAF1B-3
long non-coding RNA
proximal tubular cell
renal interstitial fibrosis
Journal
Molecular therapy. Nucleic acids
ISSN: 2162-2531
Titre abrégé: Mol Ther Nucleic Acids
Pays: United States
ID NLM: 101581621
Informations de publication
Date de publication:
14 Mar 2023
14 Mar 2023
Historique:
received:
20
04
2022
accepted:
20
12
2022
entrez:
26
1
2023
pubmed:
27
1
2023
medline:
27
1
2023
Statut:
epublish
Résumé
Renal interstitial fibrosis (RIF) is a common pathological manifestation of chronic kidney diseases. Epithelial-mesenchymal transition (EMT) of tubular epithelial cells is considered a major cause of RIF. Although long non-coding RNAs (lncRNAs) are reportedly involved in various pathophysiological processes, the roles and underlying molecular mechanisms of lncRNAs in the progression of RIF are poorly understood. In this study, we investigated the function of lncRNAs in RIF. Microarray assays showed that expression of the lncRNA lnc-CHAF1B-3 (also called claudin 14 antisense RNA 1) was significantly upregulated in human renal proximal tubular cells by both transforming growth factor-β1 (TGF-β1) and hypoxic stimulation, accompanied with increased expression of EMT-related genes. Knockdown of lnc-CHAF1B-3 significantly suppressed TGF-β1-induced upregulated expression of collagen type I alpha 1, cadherin-2, plasminogen activator inhibitor-1, snail family transcriptional repressor I (SNAI1) and SNAI2. Quantitative reverse transcriptase PCR analyses of paraffin-embedded kidney biopsy samples from IgA nephropathy patients revealed lnc-CHAF1B-3 expression was correlated positively with urinary protein levels and correlated negatively with estimated glomerular filtration rate.
Identifiants
pubmed: 36700051
doi: 10.1016/j.omtn.2022.12.011
pii: S2162-2531(22)00332-8
pmc: PMC9841231
doi:
Types de publication
Journal Article
Langues
eng
Pagination
139-150Informations de copyright
© 2022 The Authors.
Déclaration de conflit d'intérêts
The authors declare that they have no competing interests.
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