MicroRNA in cardiovascular biology and disease

Wojciechowska, Anna; Braniewska, Agata; Kozar-Kamińska, Katarzyna

doi:10.17219/acem/62915

Cited by 339 publications

(272 citation statements)

References 43 publications

(79 reference statements)

Supporting

Mentioning

265

Contrasting

Unclassified

Order By: Relevance

“…microRNAs (miRNAs) are a class of single-stranded, non-coding RNAs with approximately 22 nucleotides in length. In cardiovascular system, miRNAs control functions of various cells, such as cardiomyocytes, endothelial cells, smooth muscle cells and fibroblasts [3]. Altered miRNA expression can be found in the blood of patients with acute MI, making them promising candidates for biomarkers [4].…”

Section: Introductionmentioning

confidence: 99%

Astragaloside IV Protects Rat Cardiomyocytes from Hypoxia-Induced Injury by Down-Regulation of miR-23a and miR-92a

Gong

Chang

Zhang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Astragaloside IV (AS-IV), a traditional Chinese medicine isolated from Astragalus membranaceus, has been shown to exert cardioprotective effect previously. This study aimed to reveal the effects of AS-IV on hypoxia-injured cardiomyocyte. Methods: H9c2 cells were treated with various doses of AS-IV for 24 h upon hypoxia. CCK-8 assay, flow cytometry/Western blot, and qRT-PCR were respectively conducted to measure the changes in cell viability, apoptosis, and the expression of miR-23a and miR-92a. Sprague–Dawley rats were received coronary ligation, and were administrated by various doses of AS-IV for 14 days. The infarct volume and outcome of rats followed by ligation were tested by ultrasound, arteriopuncture and nitrotetrazolium blue chloride (NBT) staining. Results: We found that 10 μg/ml of AS-IV exerted myocardioprotective effects against hypoxia-induced cell damage, as AS-IV significantly increased H9c2 cells viability and decreased apoptosis. Interestingly, the myocardioprotective effects of AS-IV were alleviated by miR-23a and/or miR-92a overexpression. Knockdown of miR-23a and miR-92a activated PI3K/AKT and MAPK/ ERK signaling pathways. Bcl-2 was a target gene for miR-23a, and BCL2L2 was a target gene for miR-92a. In the animal model of myocardial infarction (MI), AS-IV significantly reduced the infarct volume, ejection fraction (EF), shortening fraction (FS) and LV systolic pressure (LVSP), and significantly increased left ventricular end-diastolic internal diameter (LVEDd). And also, the elevated expression of miR-23a and miR-92a in MI rat was reduced by AS-IV. Conclusion: AS-IV protected cardiomyocytes against hypoxia-induced injury possibly via down-regulation of miR-23a and miR-92a, and via activation of PI3K/AKT and MAPK/ERK signaling pathways.

show abstract

Section: Introductionmentioning

confidence: 99%

Astragaloside IV Protects Rat Cardiomyocytes from Hypoxia-Induced Injury by Down-Regulation of miR-23a and miR-92a

Gong

Chang

Zhang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Recently, many microRNAs are observed to participate in macrophage foam cell formation and vascular inflammation in atherosclerosis (Wojciechowska, Braniewska, & Kozar‐Kaminska, ). For instance, miR‐150 can increase cholesterol efflux from lipid‐loaded macrophages (Li & Zhang, ).…”

Section: Discussionmentioning

confidence: 99%

MiR‐181a inhibits vascular inflammation induced by ox‐LDL via targeting TLR4 in human macrophages

Yin

2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Atherosclerosis is a kind of chronic inflammation disease with lipid accumulation in in blood vessel linings. Increasing evidence has reported that microRNAs can exert crucial roles in atherosclerosis. In previous study, miR-181a has been implicated to be abnormally expressed in atherosclerosis mice, however its detailed function in atherosclerosis remains uninvestigated. Hence, in our current study, we focused on the biological role of miR-181a in atherosclerosis progression. Ox-LDL has been commonly identified as an important atherosclerosis regulator. We observed that ox-LDL induced THP-1 cell apoptosis dose-dependently and time- dependently. Meanwhile, 25 µg/ml ox-LDL can promote foam cell formation and increased miR-181a expression significantly. CD36 has been involved in atherosclerosis progression and it was found that overexpression of miR-181a inhibited its protein levels. Moreover, miR-181a mimics repressed foam cell formation, TC and TG levels induced by ox-LDL dramatically. In addition, miR-181a mimics were able to reverse THP-1 cell apoptosis, increased IL-6, IL-1β, and TNF-α protein expression triggered by 25 µg/ml ox-LDL. TLR4 has been linked to various inflammation-associated diseases. In our present study, TLR4 was indicated as miR-181a target and the binding correlation between them was validated by dual-luciferase reporter assay. In conclusion, these results improves the understanding of atherosclerosis modulated by miR-181a/TLR4 and can contribute to development of new approaches for atherosclerosis.

show abstract

“…19 The role of miRNAs in the pathogenesis of CVDs has been reported in many studies. 20 In terms of mechanistic actions of ln-cRNAs, lncRNAs can function as the competing endogenous RNAs (ceRNAs) for miRNAs, which in turn suppress the expression of targeted miRNAs. For example, lncRNA urothelial cancer associated 1 acts as ceRNA for miR-26a to regulate VSMC proliferation and migration.…”

Section: Micrornas (Mirnas) Also Belong To the Family Of Non-codingmentioning

confidence: 99%

“…MicroRNAs (miRNAs) also belong to the family of non‐coding RNAs and have 21‐23 nucleotides in length, and miRNAs exerted transcriptional repression on the targeted genes via forming the imperfect binding with 3′ untranslated region (3′UTR) of the targeted genes . The role of miRNAs in the pathogenesis of CVDs has been reported in many studies . In terms of mechanistic actions of lncRNAs, lncRNAs can function as the competing endogenous RNAs (ceRNAs) for miRNAs, which in turn suppress the expression of targeted miRNAs.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR‐205 and modulating Smad2

Lin

Tian

Zhang

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

The present study investigated the role of long non‐coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) in the human aortic smooth muscle cell (HASMC) proliferation and migration and explored the potential link between SNHG16 and atherosclerosis. Our results showed that platelet‐derived growth factor (PDGF)‐bb treatment promoted cell proliferation and migration with concurrent up‐regulation of SNHG16 in HASMCs. Small nucleolar RNA host gene 16 overexpression promoted HASMC proliferation and migration, while SNHG16 knockdown suppressed cell proliferation and migration in PDGF‐bb‐stimulated HASMCs. The bioinformatic analyses showed that SNHG16 possessed the complementary binding sequence with miR‐205, where the interaction was confirmed by luciferase reporter assay and RNA pull‐down assay in HASMCs, and SNHG16 inversely regulated miR‐205 expression. MiR‐205 overexpression attenuated the enhanced effects of PDGF‐bb treatment on HASMC proliferation and migration. Moreover, Smad2 was targeted and inversely regulated by miR‐205, while being positively regulated by SNHG16 in HASMCs. Smad2 knockdown attenuated PDGF‐bb‐mediated actions on HASMC proliferation and migration. Both miR‐205 overexpression and Smad2 knockdown partially reversed the effects of SNHG16 overexpression on HASMC proliferation and migration. Moreover, SNHG16 and Smad2 mRNA were up‐regulated, while miR‐205 was down‐regulated in the plasma from patients with atherosclerosis. Small nucleolar RNA host gene 16 expression was inversely correlated with miR‐205 expression and positively correlated with Smad2 expression in the plasma from atherosclerotic patients. In conclusion, our data showed the up‐regulation of SNHG16 in pathogenic‐stimulated HASMCs and clinical samples from atherosclerotic patients. Small nucleolar RNA host gene 16 regulated HASMC proliferation and migration possibly via regulating Smad2 expression by acting as a competing endogenous RNA for miR‐205.

show abstract

MicroRNA in cardiovascular biology and disease

Cited by 339 publications

References 43 publications

Astragaloside IV Protects Rat Cardiomyocytes from Hypoxia-Induced Injury by Down-Regulation of miR-23a and miR-92a

Astragaloside IV Protects Rat Cardiomyocytes from Hypoxia-Induced Injury by Down-Regulation of miR-23a and miR-92a

MiR‐181a inhibits vascular inflammation induced by ox‐LDL via targeting TLR4 in human macrophages

Long non‐coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR‐205 and modulating Smad2

Contact Info

Product

Resources

About