Correlations between vitronectin, miR-520, and miR-34 in patients with stenosis of coronary arteries.
Aged
Cell Movement
/ physiology
Constriction, Pathologic
/ pathology
Coronary Angiography
/ methods
Coronary Restenosis
/ metabolism
Coronary Stenosis
/ genetics
Coronary Vessels
/ metabolism
Female
Gene Expression
/ genetics
Humans
Hyperplasia
/ pathology
Iran
Male
MicroRNAs
/ genetics
Middle Aged
Muscle, Smooth, Vascular
/ metabolism
Neointima
/ pathology
Signal Transduction
/ physiology
Stents
/ adverse effects
Transcriptome
/ genetics
Vitronectin
/ genetics
Gene expression
Stenosis
Vitronectin
miR-193
miR-34
miR-520
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
26
08
2021
accepted:
07
10
2021
pubmed:
16
10
2021
medline:
1
3
2022
entrez:
15
10
2021
Statut:
ppublish
Résumé
In-stent restenosis usually occurs by platelet activation, neointima formation, VSMC migration, and proliferation in the position of the vessel stent. The monocytes have a magnificent role in neointimal hyperplasia since these cells recruit to the site of vessel injury through chemokines and other secretion proteins. This study is focused on the investigation of vitronectin, miR-193, miR-34, and miR-520 expression levels in PBMCs isolated from stenosed patients. A total of sixty subjects undergoing coronary artery angiography containing patients with stent no restenosis (n = 20), in-stent restenosis (n = 20), and healthy participants (n = 20) participated in the study. The vitronectin, miR-193, miR-34, and miR-520 expression levels were measured by the RT-qPCR technique. Data were analyzed by SPSS software. The vitronectin, miR-34, and miR-520 expression levels changed significantly in patients with vessel in-stent restenosis (p = 0.02, p = 0.02, and p = 0.01, respectively). Furthermore, there were inverse correlations between the expression levels of vitronectin gene and miR-34 (r = - 0.44, p = 0.04) as well as miR-520 (r = - 0.5, p=0.01). The molecular events in the vessel stenosis may be affected by targeting vitronectin with miR-520 and miR-34.
Sections du résumé
BACKGROUND
BACKGROUND
In-stent restenosis usually occurs by platelet activation, neointima formation, VSMC migration, and proliferation in the position of the vessel stent. The monocytes have a magnificent role in neointimal hyperplasia since these cells recruit to the site of vessel injury through chemokines and other secretion proteins. This study is focused on the investigation of vitronectin, miR-193, miR-34, and miR-520 expression levels in PBMCs isolated from stenosed patients.
METHODS
METHODS
A total of sixty subjects undergoing coronary artery angiography containing patients with stent no restenosis (n = 20), in-stent restenosis (n = 20), and healthy participants (n = 20) participated in the study. The vitronectin, miR-193, miR-34, and miR-520 expression levels were measured by the RT-qPCR technique. Data were analyzed by SPSS software.
RESULTS
RESULTS
The vitronectin, miR-34, and miR-520 expression levels changed significantly in patients with vessel in-stent restenosis (p = 0.02, p = 0.02, and p = 0.01, respectively). Furthermore, there were inverse correlations between the expression levels of vitronectin gene and miR-34 (r = - 0.44, p = 0.04) as well as miR-520 (r = - 0.5, p=0.01).
CONCLUSIONS
CONCLUSIONS
The molecular events in the vessel stenosis may be affected by targeting vitronectin with miR-520 and miR-34.
Identifiants
pubmed: 34652615
doi: 10.1007/s11033-021-06821-z
pii: 10.1007/s11033-021-06821-z
doi:
Substances chimiques
MIRN34 microRNA, human
0
MIRN520 microRNA, human
0
MicroRNAs
0
Vitronectin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
7913-7920Subventions
Organisme : Iran University of Medical Sciences
ID : 14442
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature B.V.
Références
Kim MJ, Jung SK (2020) Nutraceuticals for prevention of atherosclerosis: targeting monocyte infiltration to the vascular endothelium. J Food Biochem 44(3):e13200
pubmed: 32189369
Wu M-Y et al (2017) New insights into the role of inflammation in the pathogenesis of atherosclerosis. Int J Mol Sci 18(10):2034
doi: 10.3390/ijms18102034
Geovanini GR, Libby P (2018) Atherosclerosis and inflammation: overview and updates. Clin Sci 132(12):1243–1252
doi: 10.1042/CS20180306
Spadaccio C, Benedetto U (2018) Coronary artery bypass grafting (CABG) vs. percutaneous coronary intervention (PCI) in the treatment of multivessel coronary disease: quo vadis?—a review of the evidences on coronary artery disease. Annals of cardiothoracic surgery 7(4):506
doi: 10.21037/acs.2018.05.17
Malik TF, Tivakaran VS (2019) Percutaneous transluminal coronary angioplasty (PTCA). StatPearls, Treasure Island
Jukema JW et al (2012) Restenosis after PCI. Part 1: pathophysiology and risk factors. Nat Rev Cardiol 9(1):53
doi: 10.1038/nrcardio.2011.132
Su Y-C, Riesbeck K (2018) Vitronectin. The complement facts book. Elsevier, Amsterdam, pp 351–360
doi: 10.1016/B978-0-12-810420-0.00033-X
Garg N et al (2010) Plasminogen activator inhibitor-1 and vitronectin expression level and stoichiometry regulate vascular smooth muscle cell migration through physiological collagen matrices. J Thromb Haemost 8(8):1847–1854
doi: 10.1111/j.1538-7836.2010.03907.x
Luo M et al (2017) Plasminogen activator inhibitor-1 regulates the vascular expression of vitronectin. J Thromb Haemost 15(12):2451–2460
doi: 10.1111/jth.13869
Grad E et al (2018) The role of monocyte subpopulations in vascular injury following partial and transient depletion. Drug Deliv Trans Res 8(4):945–953
doi: 10.1007/s13346-017-0404-5
Yin R-X, Yang D-Z, Wu J-Z (2014) Nanoparticle drug-and gene-eluting stents for the prevention and treatment of coronary restenosis. Theranostics 4(2):175
doi: 10.7150/thno.7210
Shafiee S et al (2017) Vitronectin and urokinase-type plasminogen activator gene expression levels are increased in patients with coronary artery in-stent restenosis. Int J Angiol 26(4):218
doi: 10.1055/s-0037-1601871
Kakavandi N et al (2021) Prostaglandin E2 (PGE2) synthesis pathway is involved in coronary artery stenosis and restenosis. Gene 765:145131
doi: 10.1016/j.gene.2020.145131
Rezaee S et al (2020) COX and PTGDS gene expression levels in PGD2 synthesis pathway are correlated with miR-520 in patients with vessel restenosis. Endocr, Metab Immune Disord-Drug Targets 20(9):1514–1522
doi: 10.2174/1871530320666200511012142
Collado A et al (2021) MicroRNA: a mediator of diet-induced cardiovascular protection. Curr Opin Pharmacol 60:183–192
doi: 10.1016/j.coph.2021.07.022
Jiao Y et al (2021) MicroRNA-520c-3p suppresses vascular endothelium dysfunction by targeting RELA and regulating the AKT and NF-κB signaling pathways. Journal Physiol Biochem 77(1):47–61
doi: 10.1007/s13105-020-00779-5
Wu Z et al (2020) MiR-193-3p attenuates the vascular remodeling in pulmonary arterial hypertension by targeting PAK4. Pulm Circ 10(4):2045894020974919
pubmed: 33354317
pmcid: 7734527
Badacz R et al (2021) Expression of miR-1-3p, miR-16-5p and miR-122-5p as possible risk factors of secondary cardiovascular events. Biomedicines 9(8):1055
doi: 10.3390/biomedicines9081055
Fukuda D et al (2004) Circulating monocytes and in-stent neointima after coronary stent implantation. J Am Coll Cardiol 43(1):18–23
doi: 10.1016/j.jacc.2003.08.026
Fishman RF et al (1992) Long-term results of directional coronary atherectomy: predictors of restenosis. J Am Coll Cardiol 20(5):1101–1110
doi: 10.1016/0735-1097(92)90365-T
Gürlek A et al (1995) Restenosis after transluminal coronary angioplasty: a risk factor analysis. Eur J Cardiovasc Prev Rehabil 2(1):51–55
doi: 10.1177/174182679500200108
Violaris AG, Melkert R, Serruys PW (1994) Influence of serum cholesterol and cholesterol subfractions on restenosis after successful coronary angioplasty. A quantitative angiographic analysis of 3336 lesions. Circulation 90(5):2267–2279
doi: 10.1161/01.CIR.90.5.2267
Yaghoubi A et al (2015) Correlation of serum levels of vitronectin, malondialdehyde and Hs-CRP with disease severity in coronary artery disease. J Cardiovasc Thorac Res 7(3):113
doi: 10.15171/jcvtr.2015.24
Ekmekci H et al (2002) Plasma vitronectin levels in patients with coronary atherosclerosis are increased and correlate with extent of disease. J Thromb Thrombolysis 14(3):221–225
doi: 10.1023/A:1025000810466
Chu Y, Bucci JC, Peterson CB (2020) Identification of a PAI-1‐binding site within an intrinsically disordered region of vitronectin. Protein Sci 29(2):494–508
doi: 10.1002/pro.3770
Liu P, Wilson MJ (2012) miR-520c and miR-373 target mTOR and SIRT1, activate the Ras/Raf/MEK/Erk pathway and NF-κB, with up-regulation of MMP9 in human fibrosarcoma cells. J Cell Physiol 227(2):867
doi: 10.1002/jcp.22993
Yi M et al (2016) miR-520e regulates cell proliferation, apoptosis and migration in breast cancer. Oncol Lett 12(5):3543–3548
doi: 10.3892/ol.2016.5085
Choe N et al (2015) The microRNA miR-34c inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia by targeting stem cell factor. Cell Signal 27(6):1056–1065
doi: 10.1016/j.cellsig.2014.12.022
Hermeking H (2010) The miR-34 family in cancer and apoptosis. Cell Death Differ 17(2):193–199
doi: 10.1038/cdd.2009.56
Lin JM et al (2021. May) BCL-6 promotes the methylation of miR‐34a by recruiting EZH2 and upregulating CTRP9 to protect ischemic myocardial injury. BioFactors 47(3):386–402
doi: 10.1002/biof.1704
Gacoń J et al (2018) Diagnostic and prognostic micro-RNAs in ischaemic stroke due to carotid artery stenosis and in acute coronary syndrome: a four-year prospective study. Kardiol Polska 76(2):362–369
doi: 10.5603/KP.a2017.0243