&lt;p&gt;Carvedilol Alters Circulating MiR-1 and MiR-214 in Heart Failure&lt;/p&gt;

Shirazi-Tehrani, Elham; Firouzabadi, Negar; Tamaddon, Gholamhossein; Bahramali, Ehsan; Vafadar, Asma

doi:10.2147/pgpm.s263740

Cited by 12 publications

(5 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, little is known of the use of pegcetacopla in the treatment of heart disease. Carvedilol is one of the calcium channel blockers, and it could alter circulating miR-1 and miR-214, which are suggested in the processes of myocyte hypertrophy and apoptosis and release myocardial fibrosis [ 53 , 54 ]. In addition, it can provide prevention of chemotherapy-related cardiotoxicity [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation

Guan

Liu

Huang

et al. 2022

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

Background. Transforming growth factor beta-induced protein (TGFBI, encoded by TGFBI gene), is an extracellular matrix protein, widely expressed in variety of tissues. It binds to collagens type I, II, and IV and plays important roles in the interactions of cell with cell, collagen, and matrix. It has been reported to be associated with myocardial fibrosis, and the latter is an important pathophysiologyical basis of atrial fibrillation (AF). However, the mechanism of TGFBI in AF remains unclear. We aimed to detect the potential mechanism of TGFBI in AF via bioinformatics analysis. Methods. The microarray dataset of GSE115574 was examined to detect the genes coexpressed with TGFBI from 14 left atrial tissue samples of AF patients. TGFBI coexpression genes were then screened using the R package. Using online analytical tools, we determined the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, Gene Ontology (GO) annotation, and protein-protein interaction (PPI) network of TGFBI and its coexpression genes. The modules and hub genes of the PPI-network were then identified. Another dataset, GSE79768 was examined to verify the hub genes. DrugBank was used to detect the potential target drugs. Results. In GSE115574 dataset, a total of 1818 coexpression genes (769 positive and 1049 negative) were identified, enriched in 120 biological processes (BP), 38 cellular components (CC), 36 molecular functions (MF), and 39 KEGG pathways. A PPI-network with average 12.2-degree nodes was constructed. The genes clustered in the top module constructed from this network mainly play a role in PI3K-Akt signaling pathway, viral myocarditis, inflammatory bowel disease, and platelet activation. CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 were identified and finally verified as the hub genes, mainly enriched in pathways like leukocyte transendothelial migration, PI3K-Akt signaling pathway, viral myocarditis, rheumatoid arthritis, and platelet activation. Pegcetacoplan, ocriplasmin, and carvedilol were the potential target drugs. Conclusions. We used microdataset to identify the potential functions and mechanisms of the TGFBI and its coexpression genes in AF patients. Our findings suggest that CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 may be the hub genes.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation

Guan

Liu

Huang

et al. 2022

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

show abstract

“…miR expressions apart from their role in the pathophysiology would nominate them as emerging noninvasive biomarkers in diagnosis, treatment surveillance and prognosis in many malignancies [29] such as B-ALL.…”

Section: Discussionmentioning

confidence: 99%

“…Oncogenic miRs which are upregulated in malignancies, and tumor suppressor miRs that are downregulated in carcinogenic situations [28]. Alteration in miR expressions apart from their role in the pathophysiology would nominate them as emerging noninvasive biomarkers in diagnosis, treatment surveillance and prognosis in many malignancies [29] such as B-ALL.…”

Section: Discussionmentioning

confidence: 99%

Anticancer properties of vincristine is modulated by microRNAs in acute lymphoblastic leukemia Nalm6 cell line

Shirazi-Tehrani¹,

Vafadar

Keshavarzi³

et al. 2021

Anti-Cancer Drugs

Self Cite

View full text Add to dashboard Cite

Precursor B-cell acute lymphoblastic leukemia (B-ALL), a highly diverse disease, is the most widespread pediatric malignancy characterized by cytogenetic and molecular abnormalities such as altered microRNA (miR) expression signatures. MiRs are a class of short noncoding RNAs. Dysregulation in the expression of miRs plays a crucial role in different types of cancers. Vincristine is an antineoplastic drug with a broad spectrum of activity against different hematologic malignancies and is the firstline treatment for B-ALL. Previous studies have proposed miR-17 and miR-181/b as oncomirs and miR-34/a as a tumor suppressor in Nalm6 cells, thus in the current study, we investigated the effects of vincristine treatment on the expression of miR-17, miR-34/a and miR-181/b expression levels. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was conducted to estimate the optimal concentration of vincristine in the Nalm-6 cell line. Expression of miRs was calculated using real-time PCR. Our results showed significant downregulation of miR-17 (FC = 0.226; P < 0.0004) in Nalm6 cells after vincristine treatment. Conversely, miR-34/a (FC = 4.823; P < 0.0001) was significantly upregulated. Also, the expression of miR-181/b (FC = 0.156; P < 0.3465) was not significantly different between the vincristine treated group and the control group. In conclusion, it is proposed that one of the mechanisms by which vincristine improves B-ALL is by modulating the expression of specific miRs. These specific miRs will serve as good diagnostic and prognostic biomarkers. Anti-Cancer Drugs 33: e680-e685 Copyright

show abstract

“…miRNAs which are most abundant in the skeletal or heart muscle, are the so-called myomiRs [ 48 ]. miR-1, miR-133, miR-208 and miR-499 are among the most widely investigated miRNAs in cardiac pathologies [ 49 , 50 ].…”

Section: A Brief History and Applications Of Ncrnasmentioning

confidence: 99%

ncRNAs and polyphenols: new therapeutic strategies for hypertension

et al. 2022

Self Cite

View full text Add to dashboard Cite

Polyphenols have gained significant attention in protecting several chronic diseases, such as cardiovascular diseases (CVDs). Accumulating evidence indicates that polyphenols have potential protective roles for various CVDs. Hypertension (HTN) is among the hazardous CVDs accounting for nearly 8.5 million deaths worldwide. HTN is a complex and multifactorial disease and a combination of genetic susceptibility and environmental factors play major roles in its development. However, the underlying regulatory mechanisms are still elusive. Polyphenols have shown to cause favourable and beneficial effects in the management of HTN. Noncoding RNAs (ncRNAs) as influential mediators in modulating the biological properties of polyphenols, have shown significant footprints in CVDs. ncRNAs control basic functions in virtually all cell types relevant to the cardiovascular system and, thus, a direct link with blood pressure (BP) regulation is highly probable. Recent evidence suggests that a number of ncRNAs, including main small ncRNAs, microRNAs (miRNAs) and long ncRNAs (lncRNAs), play crucial roles with respect to the antihypertensive effects of polyphenols. Indeed, targeting lncRNAs by polyphenols will be a novel and promising strategy in the management of HTN. Herein, we reviewed the effects of polyphenols in HTN. Additionally, we emphasized on the potential effects of polyphenols on regulations of main ncRNAs, which imply the role of polyphenols in regulating ncRNAs in order to exert protective effects and thus proposing them as new targets for HTN treatment. Abbreviations : CVD: cardiovascular disease; BP: blood pressure; HTN: hypertension, lncRNAs: long noncoding RNAs; p38-MAPK: p38-mitogenactivated protein kinase; OPCs: oligomeric procyanidins; GTP: guanosine triphosphate; ROS: reactive oxygen species; cGMP: cyclic guanosine monophosphate; SGC: soluble guanylate cyclase; PI3K: phosphatidylinositol 3-kinase; cGMP: Cyclic GMP; eNOS: endothelial NO synthase; ERK ½: extracellular signal-regulated kinase ½; L-Arg: L-Arginine; MAPK: mitogen-activated protein kinases; NO: Nitric oxide; P: Phosphorus; PDK1: Phosphoinositide-dependent kinase 1; PI3-K: Phosphatidylinositol 3-kinase; PIP2: Phosphatidylinositol diphosphate; ncRNAs: non-protein-coding RNA; miRNAs: microRNAs; OPCs: oligomeric procyanidins; RES: resveratrol; GE: grape extract; T2DM: type 2 diabetes mellitus; IL: interleukin; TNF-α: tumour necrosis factor-alpha; NF-κB: nuclear factor NF-kappa-B; ALP: alkaline phosphatase; PARP1: poly [ADP-ribose] polymerase 1; HIF1a: Hypoxia-inducible-factor 1A; NFATc2: nuclear factor of activated T cells 2; PAD: peripheral artery disease; SHR: spontaneously hypertensive rat; RAAS: renin-angiotensin-aldosterone system; AT 1 R: angiotensin type-1 receptor; Nox: NADPH oxidase; HO-1: haem oxygenase-1; JAK/STAT: Janus kinase/signal transducers/activators of the transcription; PNS: panax notoginseng saponin; snoRNA: small nucleolar RNA; hnRNA: heterogeneous nuclear RNA;...

show abstract

<p>Carvedilol Alters Circulating MiR-1 and MiR-214 in Heart Failure</p>

Cited by 12 publications

References 64 publications

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation

Anticancer properties of vincristine is modulated by microRNAs in acute lymphoblastic leukemia Nalm6 cell line

ncRNAs and polyphenols: new therapeutic strategies for hypertension

Contact Info

Product

Resources

About