Inhibition of microRNA-23b prevents polymicrobial sepsis-induced cardiac dysfunction by modulating TGIF1 and PTEN

Zhang, Haiju; Caudle, Yi; Shaikh, Aamir; Yao, Baozhen; Yin, Deling

doi:10.1016/j.biopha.2018.04.092

Cited by 32 publications

(24 citation statements)

References 51 publications

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“…4,[25][26][27] In this study, we observed the obvious increase of fibrosis in atrial appendage tissue of patients with sinus rhythm, along with the significant elevation of COL1A1, COL3A1 and ACTA2. [18][19][20] Additionally, no significant effects on cell proliferation and migration were observed in HAFs with overexpression of miR-23b-3p and miR-27b-3p respectively. 28 Some miRNAs, such as miR-21 [12][13][14][15] and miR-26, 16,17 are involved in the modulation of atrial fibrosis.…”

Section: Discussionmentioning

confidence: 90%

“…These results were supported by previous reports that miR-23b and miR-27b enhance myocardial fibrosis. [18][19][20] Additionally, no significant effects on cell proliferation and migration were observed in HAFs with overexpression of miR-23b-3p and miR-27b-3p respectively.…”

Section: Discussionmentioning

confidence: 90%

“…7 Recently, more than 5000 miRNAs have been discovered in the human genome. 18 The effects of miR-27b on cardiac fibrosis are controversial. [9][10][11] It has been found that miRNA can also participate in the development of atrial fibrillation through fibrosis-related target genes.…”

Section: Introductionmentioning

confidence: 99%

“…Inhibition of miR-23b could alleviate cardiac fibrosis in caecal ligation puncture (CLP)-induced late sepsis by targeting TGIF1 and PTEN to activate TGF-β1/Smad2/3 signalling and AKT/N-Cadherin signalling in cardiac fibroblasts respectively. 18 The effects of miR-27b on cardiac fibrosis are controversial. Overexpression of miR-27b in cardiomyocytes was reported to contribute to cardiac dysfunction with enhanced myocardial fibrosis by targeting PPARγ 19 and MMP13 20 respectively.…”

Section: Introductionmentioning

confidence: 99%

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Novel role of the clustered miR‐23b‐3p and miR‐27b‐3p in enhanced expression of fibrosis‐associated genes by targeting TGFBR3 in atrial fibroblasts

Yang

Zhang

Guo³

et al. 2019

J Cellular Molecular Medi

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Atrial fibrillation (AF) is the most common type of arrhythmia in cardiovascular diseases. Atrial fibrosis is an important pathophysiological contributor to AF. This study aimed to investigate the role of the clustered miR‐23b‐3p and miR‐27b‐3p in atrial fibrosis. Human atrial fibroblasts (HAFs) were isolated from atrial appendage tissue of patients with sinus rhythm. A cell model of atrial fibrosis was achieved in Ang‐II‐induced HAFs. Cell proliferation and migration were detected. We found that miR‐23b‐3p and miR‐27b‐3p were markedly increased in atrial appendage tissues of AF patients and in Ang‐II‐treated HAFs. Overexpression of miR‐23b‐3p and miR‐27b‐3p enhanced the expression of collagen, type I, alpha 1 (COL1A1), COL3A1 and ACTA2 in HAFs without significant effects on their proliferation and migration. Luciferase assay showed that miR‐23b‐3p and miR‐27b‐3p targeted two different sites in 3ʹ‐UTR of transforming growth factor (TGF)‐β1 receptor 3 (TGFBR3) respectively. Consistently, TGFBR3 siRNA could increase fibrosis‐related genes expression, along with the Smad1 inactivation and Smad3 activation in HAFs. Additionally, overexpression of TGFBR3 could alleviate the increase of COL1A1, COL3A1 and ACTA2 in HAFs after transfection with miR‐23b‐3p and miR‐27b‐3p respectively. Moreover, Smad3 was activated in HAFs in response to Ang‐II treatment and inactivation of Smad3 attenuated up‐regulation of miR‐23b‐3p and miR‐27b‐3p in Ang‐II‐treated HAFs. Taken together, these results suggest that the clustered miR‐23b‐3p and miR‐27b‐3p consistently promote atrial fibrosis by targeting TGFBR3 to activate Smad3 signalling in HAFs, suggesting that miR‐23b‐3p and miR‐27b‐3p are potential therapeutic targets for atrial fibrosis.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Novel role of the clustered miR‐23b‐3p and miR‐27b‐3p in enhanced expression of fibrosis‐associated genes by targeting TGFBR3 in atrial fibroblasts

Yang

Zhang

Guo³

et al. 2019

J Cellular Molecular Medi

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“…In another study, miR-23b is proposed as an essential contributor to cardiac brosis activation to mediate the development of myocardial dysfunction in late sepsis. This report suggests that blocking miR-23b expression might be an effective approach to prevent sepsis-induced cardiac dysfunction [17]. Another study reveals that miR-23b inhibition downregulates the expression of programmed death ligand-1 (PD-L1) on splenic T lymphocytes of septic mice.…”

Section: Introductionmentioning

confidence: 80%

miRNA-23b as a biomarker of culture-positive neonatal sepsis

Fatmi¹,

Rebiahi

Chabni

et al. 2020

Preprint

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Background: Neonatal sepsis remains an important cause of morbidity and mortality. The ability to quickly and accurately diagnose neonatal sepsis based on clinical assessments and laboratory blood tests remains difficult, where haemoculture is the gold standard for detecting bacterial sepsis in blood culture. It is also very difficult to study because neonatal samples are lacking. Methods : Forty-eight newborns suspected of sepsis admitted to the Neonatology Department of the Mother-Child Specialized Hospital of Tlemcen. From each newborn, a minimum of 1-2 ml of blood was drawn by standard sterile procedures for blood culture. The miRNA-23b level in haemoculture was evaluated by RT-qPCR. Results : miR-23b levels increased in premature and full-term newborns in early onset sepsis ( p < 0.001 and p < 0.005 respectively), but lowered in late onset sepsis in full-term neonates ( p < 0.05) compared to the respective negative controls. miR-23b levels also increased in late sepsis in the negative versus early sepsis negative controls ( p < 0.05). miR-23b levels significantly lowered in the newborns who died from both sepsis types ( p < 0.0001 and p < 0.05 respectively). In early sepsis, miR-23b and death strongly and negatively correlated (correlation coefficient = -0.96, p = 0.0019). In late sepsis, miRNA-23b and number of survivors (correlation coefficient = 0.70, p = 0.506) positively correlated. Conclusions : Lowering miR-23b levels is an important factor that favours sepsis development, which would confirm their vital protective role, and strongly suggest that they act as a good marker in molecular diagnosis and patient monitoring.

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LncRNA TUG1 acts as a competing endogenous RNA to mediate CTGF expression by sponging miR‐133b in myocardial fibrosis after myocardial infarction

Zhang

Wang

et al. 2021

Cell Biology International

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Myocardial fibrosis (MF) is one of the basic causes of many cardiovascular diseases. Noncoding RNAs (ncRNAs), including microRNA (miRNA) and long noncoding RNA (lncRNA), have been reported to play an indispensable role in MF. The current work is focused on investigating the biological role of lncRNA taurine upregulation gene 1 (TUG1) in activating cardiac myofibroblasts as well as the underlying mechanism. The outcome revealed that after myocardial infarction TUG1 expression increased and miR‐133b expression decreased in the rat model of MF. The expression level of TUG1 increased following AngII treatment in cardiac myofibroblast. TUG1 knockdown inhibited the Ang‐II induced cardiac myofibroblast activation and TUG1 overexpression increased proliferation and collagen generation of cardiac myofibroblasts. Bioinformatic prediction programs predicted that TUG1 had MRE directly combined with miR‐133b seed sequence, luciferase activity, and RIP experiments indicated that TUG1, acted as a sponger and interacted with miR‐133b in cardiac myofibroblasts. Furthermore, a target of miR‐133b was CTGF and CTGF knockdown counteracted the promotion of MF by miR‐133b knockdown. Collectively, our study suggested that TUG1 mediates CTGF expression by sponging miR‐133b in the activation of cardiac myofibroblasts. The current work reveals a unique role of the TUG1/miR‐133b/CTGF axis in MF, thus suggesting its immense therapeutic potential in the treatment of cardiac diseases.

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Inhibition of microRNA-23b prevents polymicrobial sepsis-induced cardiac dysfunction by modulating TGIF1 and PTEN

Cited by 32 publications

References 51 publications

Novel role of the clustered miR‐23b‐3p and miR‐27b‐3p in enhanced expression of fibrosis‐associated genes by targeting TGFBR3 in atrial fibroblasts

Novel role of the clustered miR‐23b‐3p and miR‐27b‐3p in enhanced expression of fibrosis‐associated genes by targeting TGFBR3 in atrial fibroblasts

miRNA-23b as a biomarker of culture-positive neonatal sepsis

LncRNA TUG1 acts as a competing endogenous RNA to mediate CTGF expression by sponging miR‐133b in myocardial fibrosis after myocardial infarction

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