Stem cell depletion by inflammation-associated miR-155

Teramura, Takeshi; Onodera, Yuta

doi:10.18632/aging.101374

Cited by 4 publications

(4 citation statements)

References 7 publications

(11 reference statements)

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“…Taken together, the results of the present study indicated that the inhibition of miR-155 expression improved the outcomes of myocardial iri through mediating BAG5 and the MAPK signaling pathway. miR-155, as a multifunctional RNA, has been identified to function in numerous pathological and physiological processes including viral infection (37), hematopoietic lineage differentiation (38), cardiovascular disease (39), immunity (40), cancer (41), inflammation (42) and Down syndrome (43). In the present study, it was identified that miR-155 was highly expressed in the myocardial H/r model, and that overexpression of mir-155 decreased myocardial cells activity, increased the number of apoptotic cells and increased the expression of pro-apoptotic proteins.…”

Section: Discussionmentioning

confidence: 99%

miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling

Xi¹,

Li²,

Li³

et al. 2020

Mol Med Report

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increasing evidence has indicated that mir-155 is closely associated with apoptosis, which may protect the myocardium and diminish the infarct area in myocardial ischemia reperfusion injury (iri). in addition, studies have revealed that mir-155 serves a leading role in promoting fibroblast inflammation, cardiac dysfunction and other aspects of myocardial injury. The present study aimed to uncover the function and potential biological mechanism of miR-155 in myocardial iri. The rat H9c2 myocardial cells was treated with hypoxia/reoxygenation (H/r) to simulate iri in vitro. reverse transcription-quantitative polymerase chain reaction (rT-qPcr) was used to detect the expression levels of mir-155 mrna. cell counting Kit-8 and flow cytometry assays and western blot analysis were applied to determine the biological behaviors of the H/r-treated cells. The association between miR-155 and BAG family molecular chaperone regulator 5 (BAG5) was predicted by bioinformatics software and was confirmed by dual luciferase assay. RT-qPCR and western blot analysis were used to analyze the expression of BAG5. The key proteins involved in mitogen-activated protein kinase (MaPK)/JNK signaling pathway were detected by western blot analysis. The data from the rT-qPcr assay indicated that the expression of mir-155 was markedly upregulated in the H/r model, and that downregulation of mir-155 may promote cell proliferation and inhibit cell apoptosis, and vice versa. BAG5, which was downregulated in the H/R model, was confirmed as a target of miR-155 and negatively modulated by miR-155. The key proteins involved in MaPK/JnK signaling, which were highly expressed in the H/R model, were suppressed by treatment with the miR-155 inhibitor, and overexpression of BAG5 promoted the protective effect of miR-155 inhibition on cell injury caused by H/r. in addition, the expression patterns of hypoxia-inducible factor 1-α and von Hippel-lindau were altered following different treatments. Taken together, the data from the present study indicated that miR-155 inhibition represented a potential treatment strategy to improve myocardial H/R injury, which may be associated with targeting BAG5 and inhibition of the MAPK/JnK pathway.

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Section: Discussionmentioning

confidence: 99%

miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling

Xi¹,

Li²,

Li³

et al. 2020

Mol Med Report

View full text Add to dashboard Buy / Rent full text

show abstract

“…Downregulation of this miRNA facilitates migratory cell behaviour (Lee et al, 2010). On the other hand, expression of the miRNA hsa-miR-155-5p has been reported to be associated with suppression of neural stem cell (NSC) self-renewal and promotion of cell differentiation (Teramura and Onodera, 2018). Given the importance of these genes, we believe the seventeen genes must form the key MLMi circuitry in the establishment and maintenance of pluripotency.…”

Section: Resultsmentioning

confidence: 99%

Deciphering the mRNA-lncRNA-miRNA interaction landscape in human pluripotency

Ghosh

Som

2022

Preprint

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Human embryonic stem cells offer a huge potential for the study of early human development and for application in biomedical sciences. Growing evidence has shown that besides the protein coding genes, the non-coding elements of the human genome play a crucial role in maintaining its property of self renewal and in cell fate determination. However, a clear understanding of this regulatory mechanism and the landscape of interactions between the coding and non-coding elements was still lacking. To fill in this void, we use transcriptomic data from RNA-seq and small RNA-seq experiments to reconstruct the core pluripotency circuitry involving mRNAs, lncRNAs and miRNAs. The overall interaction landscape revealed an alternate circuit for the maintenance of pluripotency devoid of the classic pluripotency transcription factors NANOG, SOX2 and POU5F1. We also identified networks specific to the naive and primed states of human pluripotency revealing a new set of transcriptomic markers that could not only be used to differentiate pluripotent state from non-pluripotent state but also to identify the intra-pluripotency state. The lncRNA DANT1 was found to be crucial in determination to the two pluripotency states as it formed a bridge between the naive and primed state specific pluripotency networks. Further, we also identified and computationally validated putative ceRNA mechanism involving DANT1, the miRNAs hsa-miR-30c-2-3p, hsa-miR-210-3p and hsa-let-7b-5p, and several key pluripotency related genes including PTPRZ1, SALL2, TOX3, ZNF695, and ZYG11A which warrants further experimental validation.

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“…Chronic inflammation is considered a main factor accelerating the deterioration of stem cell function with transforming growth factor (TGF)-β and ROS accumulation as important pathological factors (Oh et al, 2014). miRNA-155 is upregulated in aging and has been suggested to contribute to inflammation-associated stem cell dysfunction (Teramura and Onodera, 2018). High expression of this specific miRNA has been found in CF lung epithelial cells and circulating neutrophils (Bhattacharyya et al, 2011).…”

Section: Stem Cell Exhaustionmentioning

confidence: 99%

Cystic Fibrosis Lung Disease in the Aging Population

et al. 2021

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The demographics of the population with cystic fibrosis (CF) is continuously changing, with nowadays adults outnumbering children and a median predicted survival of over 40 years. This leads to the challenge of treating an aging CF population, while previous research has largely focused on pediatric and adolescent patients. Chronic inflammation is not only a hallmark of CF lung disease, but also of the aging process. However, very little is known about the effects of an accelerated aging pathology in CF lungs. Several chronic lung disease pathologies show signs of chronic inflammation with accelerated aging, also termed “inflammaging”; the most notable being chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). In these disease entities, accelerated aging has been implicated in the pathogenesis via interference with tissue repair mechanisms, alterations of the immune system leading to impaired defense against pulmonary infections and induction of a chronic pro-inflammatory state. In addition, CF lungs have been shown to exhibit increased expression of senescence markers. Sustained airway inflammation also leads to the degradation and increased turnover of cystic fibrosis transmembrane regulator (CFTR). This further reduces CFTR function and may prevent the novel CFTR modulator therapies from developing their full efficacy. Therefore, novel therapies targeting aging processes in CF lungs could be promising. This review summarizes the current research on CF in an aging population focusing on accelerated aging in the context of chronic airway inflammation and therapy implications.

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Stem cell depletion by inflammation-associated miR-155

Cited by 4 publications

References 7 publications

miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling

miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling

Deciphering the mRNA-lncRNA-miRNA interaction landscape in human pluripotency

Cystic Fibrosis Lung Disease in the Aging Population

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