M
Cardiac fibrosis
M3 subtype of muscarinic acetylcholine receptor (M3 receptor)
beta-site app cleaving enzyme 1 (BACE1)
microRNA-29b (miR-29b)
Journal
Cardiovascular diagnosis and therapy
ISSN: 2223-3652
Titre abrégé: Cardiovasc Diagn Ther
Pays: China
ID NLM: 101601613
Informations de publication
Date de publication:
15 Feb 2024
15 Feb 2024
Historique:
received:
20
07
2023
accepted:
24
11
2023
medline:
4
3
2024
pubmed:
4
3
2024
entrez:
4
3
2024
Statut:
ppublish
Résumé
Previous studies have confirmed that choline exerts anti-fibrotic effect in the heart by activating the M Proliferation of cardiac fibroblasts was induced by transforming growth factor (TGF)-β1 The expression of miR-29b decreased when treated with TGF-β1 (P=0.0389) and increased after choline stimulated (P=0.0001). Overexpression of miR-29b could reverse the high expression of collagen I (P<0.0001), α-SMA (P=0.0007), and CTGF (P=0.0038) induced by TGF-β1, whereas inhibition of miR-29b had a tendency to even further increase the expression of fibrosis markers. Meanwhile, inhibition of miR-29b could reverse the anti-fibrotic effect of choline, increasing the expression of collagen I (P=0.0040), α-SMA (P=0.0001), and CTGF (P=0.0185), and promoting the fibroblast proliferation and migration. Moreover, BACE1 protein level, increased after TGF-β1 treatment (P=0.0037) and reversed by overexpression of miR-29b (P=0.0493). Choline could reduce the increase of BACE1 induced by TGF-β1 (P=0.0264), and 4-diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP) increased the expression of BACE1 (P=0.0060). Furthermore, overexpression of BACE1 could reverse the protective effect of miR-29b in cardiac fibrosis, increasing the protein level of collagen I (P=0.0404). The results suggested that M
Sections du résumé
Background
UNASSIGNED
Previous studies have confirmed that choline exerts anti-fibrotic effect in the heart by activating the M
Methods
UNASSIGNED
Proliferation of cardiac fibroblasts was induced by transforming growth factor (TGF)-β1
Results
UNASSIGNED
The expression of miR-29b decreased when treated with TGF-β1 (P=0.0389) and increased after choline stimulated (P=0.0001). Overexpression of miR-29b could reverse the high expression of collagen I (P<0.0001), α-SMA (P=0.0007), and CTGF (P=0.0038) induced by TGF-β1, whereas inhibition of miR-29b had a tendency to even further increase the expression of fibrosis markers. Meanwhile, inhibition of miR-29b could reverse the anti-fibrotic effect of choline, increasing the expression of collagen I (P=0.0040), α-SMA (P=0.0001), and CTGF (P=0.0185), and promoting the fibroblast proliferation and migration. Moreover, BACE1 protein level, increased after TGF-β1 treatment (P=0.0037) and reversed by overexpression of miR-29b (P=0.0493). Choline could reduce the increase of BACE1 induced by TGF-β1 (P=0.0264), and 4-diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP) increased the expression of BACE1 (P=0.0060). Furthermore, overexpression of BACE1 could reverse the protective effect of miR-29b in cardiac fibrosis, increasing the protein level of collagen I (P=0.0404).
Conclusions
UNASSIGNED
The results suggested that M
Identifiants
pubmed: 38434562
doi: 10.21037/cdt-23-309
pii: cdt-14-01-143
pmc: PMC10904290
doi:
Types de publication
Journal Article
Langues
eng
Pagination
143-157Informations de copyright
2024 Cardiovascular Diagnosis and Therapy. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-23-309/coif). All authors report that this work was supported by National Natural Science Foundation of China. The authors have no other conflicts of interest to declare.