The expression levels of miRNAs- 27a and 23a in the peripheral blood mononuclear cells (PBMCs) and their correlation with FOXO1 and some inflammatory and anti-inflammatory cytokines in the patients with coronary artery disease (CAD)

Babaee, Mohammad; Chamani, Elham; Ahmadi, Reza; Bahreini, Elham; Balouchnejadmojarad, Tourandokht; Nahrkhalaji, Abolfazl Shokoohi; Fallah, Soudabeh

doi:10.1016/j.lfs.2020.117898

Cited by 24 publications

(18 citation statements)

References 27 publications

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“…MiR‐27a knockout could induce cardiac dysfunction by activating FoxO1 in mice 47 . Furthermore, in patients with coronary heart disease, the serum level of FoxO1 was positively correlated with miR‐27a level, both significantly increased 48 . Atorvastatin, a lipid‐lowering drug, increased cell viability, reduced the cell surface area, and caused apoptosis in H9c2 cardiomyocytes treated with angiotensin II 49 .…”

Section: Role and Molecular Mechanism Of Foxo1 In Cardiac Hypertrophymentioning

confidence: 99%

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

Chen

Cheng

2020

ESC Heart Failure

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Cardiac hypertrophy can lead to heart failure and cardiovascular events and has become a research hotspot in the field of cardiovascular disease. Despite extensive and in-depth research, the pathogenesis of cardiac hypertrophy is far from being fully understood. Increasing evidence has shown that the transcription factor forkhead box protein O 1 (FoxO1) is closely related to the occurrence and development of cardiac hypertrophy. This review summarizes the current literature on the role and molecular mechanism of FoxO1 in cardiac hypertrophy. We searched the database MEDLINE via PubMed for available evidence on the effect of FoxO1 on cardiac hypertrophy. FoxO1 has many effects on multiple diseases, including cardiovascular diseases, diabetes, cancer, aging, and stem cell activity. Recent studies have shown that FoxO1 plays a critical role in the development of cardiac hypertrophy. Evidence for this relationship includes the following. (i) FoxO1 can regulate cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy and (ii) is controlled by several upstream signalling molecules (e.g. phosphatidylinositol 3-kinase/Akt, AMP-activated protein kinase, and sirtuins) and regulates many downstream transcription proteins (e.g. ubiquitin ligases muscle RING finger 1/muscle atrophy F-box, calcineurin/nuclear factor of activated T cells, and microRNAs). In response to stress or external stimulation (e.g. low energy, oxidative stress, or growth factor signalling), FoxO1 undergoes post-translational modification and transfers from the cytoplasm to nucleus, thus regulating the expression of a series of target genes in myocardium that are involved in cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy. (iii) Finally, targeted regulation of FoxO1 is an effective method of intervening in myocardial hypertrophy. The information reviewed here should be significant for understanding the roles of FoxO1 in cardiac hypertrophy and should contribute to the design of further studies related to FoxO1 and the hypertrophic response. It should also shed light on a potential treatment for cardiac hypertrophy.

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Section: Role and Molecular Mechanism Of Foxo1 In Cardiac Hypertrophymentioning

confidence: 99%

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

Chen

Cheng

2020

ESC Heart Failure

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“…Therefore, taken together our study results might evidence, in obese patients with pre-diabetes, the implication of miR-195 and miR-27 as regulators of glucose homeostasis and insulin resistance, and of inflammation/oxidative stress pathways which are implied in cardiovascular remodeling (17)(18)(19)(20)(21)(22)(23)(24)(25). Notably and clinically relevant, the metformin in these patients could modulate these metabolic and inflammatory pathways, leading to cardio-protective effects.…”

Section: Discussionmentioning

confidence: 51%

“…Indeed, miR-27 is implied in molecular pathways regulators of lipid metabolism, vascular signaling, and glucose homeostasis (23). to reduced expression of SIRT1 (24). Notably, miR-27 has a regulatory role in increasing insulin sensitivity (25).…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs Modulation and Clinical Outcomes at 1 Year of Follow-Up After Excision of Subcutaneous Abdominal Fat in Overweight Patients with Pre-Diabetes Treated with Metformin vs. Placebo

Sardu¹,

Trotta²,

Pieretti³

et al. 2020

Preprint

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Background: obese pre-diabetics have altered expression of cytokines, and sirtuin-1, that might influence myocardial function via microRNAs (miRs) expression. Objectives: to evaluate inflammatory/oxidative stress, miRs’ expression and cardiovascular function in obese pre-diabetics randomly assigned to metformin therapy vs. placebo vs. normo-glycemics at 12 months of follow-up. Materials and methods: eighty-three obese patients enrolled for abdominoplastic surgery, were divided in pre-diabetics (n 55), normo-glycemics (n 28), and assigned to hypocaloric diet. Pre-diabetics were randomly assigned to metformin (n 23) or to placebo (n 22) plus hypocaloric diet. Results: at enrollment, pre-diabetics obese vs. normo-glycemic presented higher values of glucose, insulin resistance (HOMA-IR), inflammatory/oxidative stress markers, miR-195 and miR-27, and lower values of sirtuin-1 (p<0.05). At 12 months of follow up, obese pre-diabetics with metformin vs. placebo experienced significant reduction of glucose values, HOMA-IR, and inflammatory/oxidative stress markers, with significant reduction of intima-media thickness (IMT), septum and posterior wall thickness, and left ventricle mass (LVM), (p <0.05). At 12 months of follow-up, obese pre-diabetics with placebo vs. normo-glycemics had higher values of inflammatory/oxidative stress markers, higher values of IMT, septum and posterior wall thickness, LVM, and myocardial performance index (MPI), (p<0.05). Obese pre-diabetics in metformin vs. placebo, and obese pre-diabetics with placebo vs. normoglycemics, had significant differences about IMT, MPI, and LVM (p<0.05). Obese pre-diabetics in metformin vs. placebo showed significant reduction of serum miR-195 and miR-27 (p<0.05). Obese pre-diabetics in metformin vs. normoglycemics showed higher expression of serum miR-195 and miR-27 ( p<0.05). Finally, we found inverse relation between IMT and insulin (R -0.351), HOMA-IR (R -0.340), miR-195 (R -0.355), miR-27 (R -0.181); between LVEF and Insulin (R -0.332), HOMA-IR (R -0.142), miR-195 (R -0.297) and miR-27 (R -0.163). We found inverse correlation between LVM and sirtuin-1 (R -0.272), Insulin (R -0.810), HOMA-IR (R-0.183), miR-195 (R -0.446) and miR-27 (R-0.433), and direct correlation with interleukin-6 (R 0.195). MPI inversely linked to miR-195 (R -0.260) and miR-27 (R -0.591). Conclusion: in obese pre-diabetics metformin therapy significantly reduces inflammation/oxidative stress, circulating miR-195 and miR-27, causing reduction of LVM, IMT and amelioration of cardiac performance.

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“…Another study reported that treatment with anti-IL-6 receptor antibody was bene cial in restricting atherosclerosis provoked by dyslipidemia and in ammation (15). A novel study observed that IL-6 and TNF-α serum levels were signi cantly higher in CAD group and had a positive associated with the stenosis severity of CAD (16). In contrast, our results showed that serum levels of TNF-α and IL-32 in the CAD subjects suffering from cardiac arterial stenosis in one major vessel were signi cantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessel.…”

Section: Discussionmentioning

confidence: 97%

IL-32 Serum Levels in Coronary Artery Disease Patient and its Relationship with IL-6 and TNF-α Serum Levels

Mohammad-Rezaei¹,

Ahmadi²,

Rafiei³

et al. 2021

Preprint

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Coronary Artery Disease (CAD) is a chronic inflammatory disease caused by atherosclerosis and arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a new proinflammatory cytokine, which enhances inflammation through inducing different inflammatory cytokines. The purpose of current research was to assess IL-32 serum levels in coronary artery disease subjects and its relationship with serum levels of IL-6 and TNF-α. Forty-two subjects diagnosed with CAD and thirty-nine control subjects were enrolled in the research. Serum levels of IL-6, TNF-α, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). IL-32, TNF-α, and IL-6 serum levels were significantly higher by 2.7, 3.48, and 3.2-fold in the CAD subjects than in control subjects, respectively. Moreover, no significant difference was found in TNF-α, IL-6 and IL-32 serum levels with the clogged arteries number in the CAD group. TNF-α and IL-32 serum levels in the CAD subjects with cardiac arterial stenosis in one major vessel were significantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessels. ROC curve analysis revealed that serum levels of IL-32, TNF-α, and IL-6 showed good abilities in predicting CAD. Also, Multiple logistic regression analyses suggested that TNF-α, IL-6, and IL-32, serum levels of LDL and ox-LDL were independently related to the presence of CAD, while HDL serum levels were not. TNF-α, IL-32, and IL-6 showed an increase in CAD group and serum levels of these cytokines showed good abilities in predicting CAD. Our data suggested the involvement of TNF-α and IL-32 in the early stage of CAD.

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The expression levels of miRNAs- 27a and 23a in the peripheral blood mononuclear cells (PBMCs) and their correlation with FOXO1 and some inflammatory and anti-inflammatory cytokines in the patients with coronary artery disease (CAD)

Cited by 24 publications

References 27 publications

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

MicroRNAs Modulation and Clinical Outcomes at 1 Year of Follow-Up After Excision of Subcutaneous Abdominal Fat in Overweight Patients with Pre-Diabetes Treated with Metformin vs. Placebo

IL-32 Serum Levels in Coronary Artery Disease Patient and its Relationship with IL-6 and TNF-α Serum Levels

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