Inflammation-induced miRNA-155 inhibits self-renewal of neural stem cells via suppression of CCAAT/enhancer binding protein β (C/EBPβ) expression

Obora, Kayoko; Onodera, Yuta; Takehara, Toshiyuki; Frampton, John P.; Hasei, Joe; Ozaki, Toshifumi; Teramura, Takeshi; Fukuda, Kanji

doi:10.1038/srep43604

Cited by 23 publications

(22 citation statements)

References 81 publications

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“…To determine the mechanism by which miR-155 activates myogenic differentiation, we focused on the role of C/ebpβ. Until now, it has been well demonstrated that C/ebpβ is a direct target of miR-155-5p both in mice and humans [ 18 , 20 ]. Meanwhile, there is some evidence that C/ebpβ is an essential molecule for maintaining the undifferentiated state of MuSCs [ 27 ].…”

Section: Resultsmentioning

confidence: 99%

“…In vitro overexpression experiments clearly showed that miR-155 activated myogenic differentiation of C2C12 model cells. Regarding the function of miR-155 as a differentiation activator, we recently reported that miR-155 blocks neural stem cell self-renewal by suppressing the expression of transcription factors involved in stemness both in mouse and human cells [ 18 ]. On the other hand, Seok et al .…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs are a class of around 22-nucleotide-long noncoding RNAs that regulate gene expression at the post-transcriptional level [ 15 – 17 ]. miR-155 is a dominant inflammation-associated miRNA and is involved in stem cell differentiation and deterioration [ 18 ]. Interestingly, miR-155 is significantly upregulated in various human muscle disorders [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Inflammation-associated miR-155 activates differentiation of muscular satellite cells

et al. 2018

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Tissue renewal and muscle regeneration largely rely on the proliferation and differentiation of muscle stem cells called muscular satellite cells (MuSCs). MuSCs are normally quiescent, but they are activated in response to various stimuli, such as inflammation. Activated MuSCs proliferate, migrate, differentiate, and fuse to form multinucleate myofibers. Meanwhile, inappropriate cues for MuSC activation induce premature differentiation and bring about stem cell loss. Recent studies revealed that stem cell regulation is disrupted in various aged tissues. We found that the expression of microRNA (miR)-155, which is an inflammation-associated miR, is upregulated in MuSCs of aged muscles, and this upregulation activates the differentiation process through suppression of C/ebpβ, which is an important molecule for maintaining MuSC self-renewal. We also found that Notch1 considerably repressed miR-155 expression, and loss of Notch1 induced miR-155 overexpression. Our findings suggest that miR-155 can act as an activator of muscular differentiation and might be responsible for accelerating aging-associated premature differentiation of MuSCs.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inflammation-associated miR-155 activates differentiation of muscular satellite cells

et al. 2018

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“…The present study demonstrated that overexpression of miR-155 significantly increased TNF-α, IL-18, IL-6 and IL-1β levels in keratinocyte-induced HaCaT cells, through the NLRP3 inflammasome. Obora et al (18) described that inflammation-induced miR-155 inhibits self-renewal of neural stem cells. However, it remains to be elucidated how miR-155 regulates NLRP3 in psoriasis.…”

Section: Discussionmentioning

confidence: 99%

Silencing of miR‑155 suppresses inflammatory responses in psoriasis through inflammasome NLRP3 regulation

Luo

Zeng

et al. 2018

Int J Mol Med

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Psoriasis is a dermatosis with the major clinical symptoms of scale, erythema and itching, and it has a long disease course. In addition, it is easily recurrent and refractory, greatly affecting the physical and mental health of patients. In the present study, it was hypothesized that the function of miR‑155 increases psoriasis‑induced inflammation and that its expression may be dependent on inflammasome activation. miR‑155 expression was examined by gene chip array and quantitative polymerase chain reaction analysis. miR‑155 expression levels were significantly increased in an in vivo model of psoriasis compared with normal tissues, as was the expression of NLR family pyrin domain containing 3 (NLRP3). In vitro, using keratinocyte‑induced HaCaT cells as a model for psoriasis, silencing of miR‑155 was confirmed to significantly decrease inflammation and NLRP3/caspase‑1 signaling. Activation of toll‑like receptor 4 (TLR4) enhanced the miR‑155‑induced inflammatory response in the in vitro keratinocyte model. Treatment with a TLR4 inhibitor or an NLRP3 inhibitor reversed the miR‑155‑mediated inflammation in the same cell system. The present study demonstrated that miR‑155 silencing suppressed psoriasis‑associated inflammatory responses through inflammasome NLRP3 regulation.

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“…A vast majority of clinically diagnosed cases are in the intermediate and advanced stage due to the lack of early specific symptoms and tumor markers for early detection and diagnosis, which has led to the high mortality of gastric cancer (13). Therefore, searching for tumor markers for the early screening or diagnosis of gastric cancer, together with developing agents with high efficiency and low toxicity is of great importance (14). The discovery of miRNAs is a milestone in the field of molecular biology (3).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑495 regulates human gastric cancer cell apoptosis and migration through Akt and mTOR signaling

et al. 2018

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In the present study, we investigated the expression and cellular distribution of in human gastric cancer. Prominent downregulation of miR-495 activation was evident in patients with gastric cancer. Cell viability and Annexin V/PI apoptosis assays were used to assess cell proliferation and apoptosis. Then, western blot analysis was used to assess cyclin D1, PI3K, p-Akt and p-mTOR protein expression. Overexpression of miR-495 significantly inhibited cell proliferation, and promoted cell apoptosis of gastric cancer cells. Overexpression of miR-495 also promoted caspase-3/-9 and Bax protein expression, and suppressed cyclin D1 protein expression and the PI3K/Akt/mTOR pathway in gastric cancer cells. Downregulation of miR-495 increased cell proliferation and inhibited cell apoptosis of gastric cancer cells through activation of the PI3K/Akt/mTOR pathway. The PI3K inhibitor, was used to suppress the PI3K/Akt/mTOR pathway, inhibit cell proliferation, promote cell apoptosis, promote caspase-3/-9 and Bax protein expression, and suppress cyclin D1 protein expression of gastric cancer cells through miR-495 inhibition. In conclusion, miR-495 is an important regulator of human gastric cancer cells and may contribute to cell apoptosis through the PI3K/Akt/mTOR/Bax-caspase-3/-9 and cyclin D1 pathway.

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Inflammation-induced miRNA-155 inhibits self-renewal of neural stem cells via suppression of CCAAT/enhancer binding protein β (C/EBPβ) expression

Cited by 23 publications

References 81 publications

Inflammation-associated miR-155 activates differentiation of muscular satellite cells

Inflammation-associated miR-155 activates differentiation of muscular satellite cells

Silencing of miR‑155 suppresses inflammatory responses in psoriasis through inflammasome NLRP3 regulation

MicroRNA‑495 regulates human gastric cancer cell apoptosis and migration through Akt and mTOR signaling

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