CircPDS5B Reduction Improves Angiogenesis Following Ischemic Stroke by Regulating MicroRNA-223-3p/NOTCH2 Axis.
Journal
Neurology. Genetics
ISSN: 2376-7839
Titre abrégé: Neurol Genet
Pays: United States
ID NLM: 101671068
Informations de publication
Date de publication:
Jun 2023
Jun 2023
Historique:
received:
07
01
2023
accepted:
06
03
2023
medline:
8
5
2023
pubmed:
8
5
2023
entrez:
8
5
2023
Statut:
epublish
Résumé
Ischemic stroke (IS) is responsible for major causes of global death and disability, for which promoting angiogenesis is a promising therapeutic strategy. This study analyzed circular RNA PDS5B (circPDS5B) and its related mechanisms in angiogenesis in IS. In the permanent middle cerebral artery occlusion (pMCAO) mouse model, circPDS5B, microRNA (miR)-223-3p, and NOTCH2 levels were checked. By testing neurologic function, neuronal apoptosis, and expression of angiogenesis-related proteins in pMCAO mice, the protective effects of circPDS5B knockdown were probed. In human brain microvascular endothelial cells (HBMECs) under oxygen-glucose deprivation (OGD) conditions, the effects of circPDS5B, miR-223-3p, and NOTCH2 on angiogenesis were studied by measuring cellular activities. The increase of circPDS5B and NOTCH2 expression and the decrease of miR-223-3p expression were examined in pMCAO mice. Reducing circPDS5B expression indicated protection against neurologic dysfunction, apoptosis, and angiogenesis impairment. For circPDS5B-depleted or miR-223-3p-restored HBMECs under OGD treatment, angiogenesis was promoted. MiR-223-3p inhibition-associated reduction of angiogenesis could be counteracted by knocking down NOTCH2. CircPDS5B depletion-induced angiogenesis in OGD-conditioned HBMECs was repressed after overexpressing NOTCH2. In IS, the expression of circPDS5B was upregulated, and miR-223-3p inhibited HBMECs activity and promoted NOTCH2 expression, thus promoting IS. CircPDS5B reduction improves angiogenesis following ischemic stroke by regulating microRNA-223-3p/NOTCH2 axis.
Sections du résumé
Background and Objectives
UNASSIGNED
Ischemic stroke (IS) is responsible for major causes of global death and disability, for which promoting angiogenesis is a promising therapeutic strategy. This study analyzed circular RNA PDS5B (circPDS5B) and its related mechanisms in angiogenesis in IS.
Methods
UNASSIGNED
In the permanent middle cerebral artery occlusion (pMCAO) mouse model, circPDS5B, microRNA (miR)-223-3p, and NOTCH2 levels were checked. By testing neurologic function, neuronal apoptosis, and expression of angiogenesis-related proteins in pMCAO mice, the protective effects of circPDS5B knockdown were probed. In human brain microvascular endothelial cells (HBMECs) under oxygen-glucose deprivation (OGD) conditions, the effects of circPDS5B, miR-223-3p, and NOTCH2 on angiogenesis were studied by measuring cellular activities.
Results
UNASSIGNED
The increase of circPDS5B and NOTCH2 expression and the decrease of miR-223-3p expression were examined in pMCAO mice. Reducing circPDS5B expression indicated protection against neurologic dysfunction, apoptosis, and angiogenesis impairment. For circPDS5B-depleted or miR-223-3p-restored HBMECs under OGD treatment, angiogenesis was promoted. MiR-223-3p inhibition-associated reduction of angiogenesis could be counteracted by knocking down NOTCH2. CircPDS5B depletion-induced angiogenesis in OGD-conditioned HBMECs was repressed after overexpressing NOTCH2.
Discussion
UNASSIGNED
In IS, the expression of circPDS5B was upregulated, and miR-223-3p inhibited HBMECs activity and promoted NOTCH2 expression, thus promoting IS. CircPDS5B reduction improves angiogenesis following ischemic stroke by regulating microRNA-223-3p/NOTCH2 axis.
Identifiants
pubmed: 37152444
doi: 10.1212/NXG.0000000000200074
pii: NXG-2023-000017
pmc: PMC10162703
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e200074Informations de copyright
Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.
Déclaration de conflit d'intérêts
The authors report no disclosures relevant to the manuscript. Full disclosure form information provided by the authors is available with the full text of this article at Go to Neurology.org/NG.
Références
Exp Neurol. 2017 Sep;295:144-154
pubmed: 28602832
Adv Healthc Mater. 2021 Jun;10(12):e2100028
pubmed: 34028998
Int J Mol Sci. 2020 Feb 13;21(4):
pubmed: 32070035
Cardiovasc Toxicol. 2017 Jan;17(1):42-48
pubmed: 26717922
Biosci Rep. 2019 Mar 6;39(3):
pubmed: 30038058
Front Mol Neurosci. 2021 Feb 04;13:613976
pubmed: 33613191
Stroke. 2010 Oct;41(10 Suppl):S64-71
pubmed: 20876509
Biosci Rep. 2020 Jun 26;40(6):
pubmed: 32537657
Life Sci. 2021 Oct 1;282:119798
pubmed: 34237309
J Pers Med. 2021 Jun 04;11(6):
pubmed: 34199723
Cerebrovasc Dis. 2020;49(1):39-54
pubmed: 31927543
Eur J Neurol. 2022 Feb;29(2):486-495
pubmed: 34725884
Science. 2012 Nov 30;338(6111):1229-32
pubmed: 23197537
Int J Mol Sci. 2020 Sep 14;21(18):
pubmed: 32937836
Life Sci. 2020 Nov 1;260:118403
pubmed: 32926923
Front Pharmacol. 2020 Mar 03;11:59
pubmed: 32194396
Circulation. 2019 Mar 5;139(10):e56-e528
pubmed: 30700139
Atherosclerosis. 2020 Apr;298:14-26
pubmed: 32131039
J Cell Physiol. 2020 Mar;235(3):2609-2618
pubmed: 31502677
PLoS One. 2015 Oct 20;10(10):e0141214
pubmed: 26485708
FEBS J. 2016 May;283(9):1720-33
pubmed: 26929185
Nat Struct Mol Biol. 2009 Sep;16(9):961-6
pubmed: 19668211
J Neurosci. 2018 Jan 3;38(1):32-50
pubmed: 29114076
Neurotox Res. 2020 Oct;38(3):564-578
pubmed: 32578041
Curr Pharm Des. 2020;26(42):5533-5545
pubmed: 32534564
J Neurosci. 2019 Sep 11;39(37):7369-7393
pubmed: 31311824
Ann Card Anaesth. 2019 Oct-Dec;22(4):407-411
pubmed: 31621677
Mol Biol Rep. 2022 Jul;49(7):6779-6788
pubmed: 34410579
Clin Genet. 2019 Jan;95(1):85-94
pubmed: 29767458
Angiogenesis. 2019 May;22(2):341-354
pubmed: 30607697
Acta Neurobiol Exp (Wars). 2019;79(2):205-216
pubmed: 31342956
Oxid Med Cell Longev. 2021 Nov 08;2021:3823122
pubmed: 34790286
Curr Vasc Pharmacol. 2015;13(3):352-65
pubmed: 26156265
Bioengineered. 2021 Dec;12(1):2550-2562
pubmed: 34115574
Stroke. 2020 Jan;51(1):319-323
pubmed: 31690252