Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1

Chen, Jianfeng; Zhang, Mingming; Zhang, Shouyan; Wu, Junlong; Xue, Sheliang

doi:10.1186/s12872-020-01520-2

Cited by 16 publications

(13 citation statements)

References 36 publications

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“…In addition, overexpression of miR-30c-5p-induced protective effects are associated with its target gene Bach1 and subsequent activation of Nrf2( 48 ). However, another study found that miR-30c expression is increased in a rat model of MI/R injury and overexpression of miR-30c-5p promotes MI/R injury by activating NF-κB pathway and targeting sirtuin 1( 49 ). In the aforementioned study ( 49 ), LAD was ligated for 30 min before reperfusion for 2 h, while in the present study, following 30 min LAD ligation, hearts were reperfused for 30 min before sample collection.…”

Section: Discussionmentioning

confidence: 99%

miR‑30c reduces myocardial ischemia/reperfusion injury by targeting SOX9 and suppressing pyroptosis

Nie

Zhou

et al. 2023

Exp Ther Med

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MicroRNAs (miRNAs or miRs) are commonly involved in regulating myocardial ischemia/reperfusion (I/R) injury by binding and silencing their target genes. However, whether miRNAs regulate myocardial I/R-induced pyroptosis remains unclear. The present study established an in vivo rat model of myocardial I/R injury and in vitro hypoxia/reoxygenation (H/R) injury model in rat primary cardiomyocytes to investigate the function and the underlying mechanisms of miRNAs on I/R injury-induced pyroptosis. RNA sequencing was utilized to select the candidate miRNAs between normal and I/R group. Reverse transcription-quantitative PCR and western blotting were performed to detect candidate miRNAs (miR-30c-5p, also known as miR-30c) and SRY-related high mobility group-box gene 9 (SOX9) expression, as well as expression of pyroptosis-associated proteins (NF-κB, ASC, caspase-1, NLRP3) in the myocardial I/R model. ELISA was used to measure pyroptosis-associated inflammatory markers IL-18 and IL-1β. Moreover, the link between miR-30c and SOX9 was predicted using bioinformatics and luciferase reporter assay. In myocardial I/R injured rats, miR-30c was downregulated, while the expression of SOX9 was upregulated. Overexpression of miR-30c inhibited pyroptosis both in vivo and in vitro . Furthermore, miR-30c negatively regulated SOX9 expression by binding its 3'untranslated region. In conclusion, the miR-30c/SOX9 axis decreased myocardial I/R injury by suppressing pyroptosis, which may be a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

miR‑30c reduces myocardial ischemia/reperfusion injury by targeting SOX9 and suppressing pyroptosis

Nie

Zhou

et al. 2023

Exp Ther Med

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“…Thus, it seems that cellular miRNAs could not only serve as components of host response in maintaining homeostasis but also be taken advantage of by pathogens for their own survival. In humans, miR-30c-5p was involved in apoptosis, inflammation, autophagy, and other physiological processes by different targets, including ATG5 [ 49 ], eIF2α [ 50 ], SIRT1 [ 51 ], and FOXO3 [ 52 ]. As far as we know, this study is the first report to show that gga-miR-30c-5p is involved in FAdV-4-induced apoptosis in host cells by targeting Mcl-1, an anti-apoptotic member of the Bcl-2 family.…”

Section: Discussionmentioning

confidence: 99%

Gga-miR-30c-5p Enhances Apoptosis in Fowl Adenovirus Serotype 4-Infected Leghorn Male Hepatocellular Cells and Facilitates Viral Replication through Myeloid Cell Leukemia-1

Haiyilati

Zhou

et al. 2022

Viruses

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Fowl adenovirus serotype 4 (FAdV-4) is the primary causative agent responsible for the hepatitis-hydropericardium syndrome (HHS) in chickens, leading to considerable economic losses to stakeholders. Although the pathogenesis of FAdV-4 infection has gained attention, the underlying molecular mechanism is still unknown. Here, we showed that the ectopic expression of gga-miR-30c-5p in leghorn male hepatocellular (LMH) cells enhanced apoptosis in FAdV-4-infected LMH cells by directly targeting the myeloid cell leukemia-1 (Mcl-1), facilitating viral replication. On the contrary, the inhibition of endogenous gga-miR-30c-5p markedly suppressed apoptosis and viral replication in LMH cells. Importantly, the overexpression of Mcl-1 inhibited gga-miR-30c-5p or FAdV-4-induced apoptosis in LMH cells, reducing FAdV-4 replication, while the knockdown of Mcl-1 by RNAi enhanced apoptosis in LMH cells. Furthermore, transfection of LMH cells with gga-miR-30c-5p mimics enhanced FAdV-4-induced apoptosis associated with increased cytochrome c release and caspase-3 activation. Thus, gga-miR-30c-5p enhances FAdV-4-induced apoptosis by directly targeting Mcl-1, a cellular anti-apoptotic protein, facilitating FAdV-4 replication in host cells. These findings could help to unravel the mechanism of how a host responds against FAdV-4 infection at an RNA level.

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“…Pro-inflammatory miRNAs such as miR-22, miR-199a-214, miR-361, and miR-665 are elevated ( el Azzouzi et al, 2013 ; Wang K. et al, 2015 ; Du et al, 2016 ; Lin et al, 2019 ), whereas anti-inflammatory miRNAs such as miR-138 and miR-499-5p are reduced ( Wang J. et al, 2011 ; Zhu et al, 2017 ) to impair normal mitochondrial function in myocardial cells. In addition, abnormal expression of miR-30c-5p, miR-181c-5p, miR-327, miR-130a-5p, and miR-708 upon H/I stimulation could regulate myocardial inflammation through NF-κB signaling ( Yang et al, 2018 ; Chen et al, 2020a ; Wang S. et al, 2020 ; Zhang et al, 2020c ; Li Y. et al, 2021 ; Qu et al, 2021 ; Sun et al, 2021 ; Table 2 ). One of the key inflammatory mediators, NLRP3 inflammasome, may also be a direct target of H/I-sensitive miRNAs.…”

Section: Effects Of Hypoxia/ischemia On Micrornas In Hypoxia-sensitiv...mentioning

confidence: 99%

Hypoxic/Ischemic Inflammation, MicroRNAs and δ-Opioid Receptors: Hypoxia/Ischemia-Sensitive Versus-Insensitive Organs

Chen

Zhao

et al. 2022

Front. Aging Neurosci.

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Hypoxia and ischemia cause inflammatory injury and critically participate in the pathogenesis of various diseases in various organs. However, the protective strategies against hypoxic and ischemic insults are very limited in clinical settings up to date. It is of utmost importance to improve our understanding of hypoxic/ischemic (H/I) inflammation and find novel therapies for better prevention/treatment of H/I injury. Recent studies provide strong evidence that the expression of microRNAs (miRNAs), which regulate gene expression and affect H/I inflammation through post-transcriptional mechanisms, are differentially altered in response to H/I stress, while δ-opioid receptors (DOR) play a protective role against H/I insults in different organs, including both H/I-sensitive organs (e.g., brain, kidney, and heart) and H/I-insensitive organs (e.g., liver and muscle). Indeed, many studies have demonstrated the crucial role of the DOR-mediated cyto-protection against H/I injury by several molecular pathways, including NLRP3 inflammasome modulated by miRNAs. In this review, we summarize our recent studies along with those of others worldwide, and compare the effects of DOR on H/I expression of miRNAs in H/I-sensitive and -insensitive organs. The alternation in miRNA expression profiles upon DOR activation and the potential impact on inflammatory injury in different organs under normoxic and hypoxic conditions are discussed at molecular and cellular levels. More in-depth investigations into this field may provide novel clues for new protective strategies against H/I inflammation in different types of organs.

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Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1

Cited by 16 publications

References 36 publications

miR‑30c reduces myocardial ischemia/reperfusion injury by targeting SOX9 and suppressing pyroptosis

miR‑30c reduces myocardial ischemia/reperfusion injury by targeting SOX9 and suppressing pyroptosis

Gga-miR-30c-5p Enhances Apoptosis in Fowl Adenovirus Serotype 4-Infected Leghorn Male Hepatocellular Cells and Facilitates Viral Replication through Myeloid Cell Leukemia-1

Hypoxic/Ischemic Inflammation, MicroRNAs and δ-Opioid Receptors: Hypoxia/Ischemia-Sensitive Versus-Insensitive Organs

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