MicroRNA‐181a Regulates Local Immune Balance by Inhibiting Proliferation and Immunosuppressive Properties of Mesenchymal Stem Cells

Liu, Liu; Wang, Yaping; Fan, Hong; Zhao, Xiangfu; Liú, Dan; Hu, Yali; Kidd, Ambrose R.; Bao, Jianxin; Hou, Yayi

doi:10.1002/stem.1156

Cited by 88 publications

(75 citation statements)

References 73 publications

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“…Similar to our findings, study by Liu et al [49] and Raghu et al [52] also demonstrated that miR-181a can inhibit TGF-β signaling by directly targeting Tgfbr1 in C2C12 mesenchymal precursor cells, MC3T3 preosteoblasts and MSCs, further confirming that the regulatory role of miR-181a-5p in TECs proliferation is tightly linked to TGF-β. The negative role in the formation of thymic microenvironment and the antiproliferative role in cells of epithelial organ have been well defined for TGF-β signaling [11,53].…”

Section: Discussionsupporting

confidence: 92%

“…The inactivation of either one in the reaction chains will lead to impairment of the TGF-β-mediated cell growth and proliferation. This indicates that down-regulated Tgfbr1 expression or Smad2/3 phosphorylation will block the activation of latent TGF-β [47][48][49]. To further identify whether the TGF-β signaling is affected by the expression of miR-181a-5p in MTEC1 cells, the protein levels of p-Smad2 and p-Smad3 were measured in MTEC1 cells.…”

Section: Discussionmentioning

confidence: 99%

“…In line with our findings, Alliston et al [50] also demonstrated that TGF-β can inhibit the osteoblastic differentiation by suppressing the expression of Smad3. Additionally, Liu et al [49] indicated that the levels of p-Smad2 were also downregulated by overexpression of miR-181a in mesenchymal stem cells (MSCs). In our study, we also detected the protein levels of p-Smad2 in MTEC1 cells, but no change was observed between the mimic and mimic-NC groups.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-β signaling

Guo

et al. 2016

ABBS

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The expression profiles of miRNAs in thymus tissues from mice of different age have been demonstrated in our previous study. After an integrated analysis of the miRNA expression profiles, we demonstrated that the expression of miR-181a-5p was significantly decreased in thymic epithelial cells (TECs) from 10-to 19-month-old mice when compared with that in TECs from 1-month-old mice by quantitative reverse transcriptase polymerase chain reaction. We hypothesized that miR-181a-5p in TECs might be associated with the age-related thymus involution through regulating some genes or signaling pathway. To test this hypothesis, the mouse medullary thymic epithelial cells (MTEC1) were used. Transfection with miR-181a-5p mimic promoted the proliferation of MTEC1 cells, but did not affect apoptosis. The effect was reversed when the expression of miR-181a-5p was suppressed in MTEC1 cells. Furthermore, the transforming growth factor beta receptor I (Tgfbr1) was confirmed as a direct target of miR-181a-5p by luciferase assay. Moreover, it was found that overexpression of miR-181a-5p down-regulated the phosphorylation of Smad3 and blocked the activation of the transforming growth factor beta signaling. Nevertheless, an inversely correlation was observed between the expression of Tgfbr1 and miR-181a-5p in TECs derived from mice of different age. Collectively, we provide evidence that miR-181a-5p may be an important endogenous regulator in the proliferation of TECs, and the expression levels of miR-181a-5p in TECs may be associated with the age-related thymus involution.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-β signaling

Guo

et al. 2016

ABBS

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“…For example, previous studies showed that miR‐181a regulates local immune balance (Liu et al ., 2012) and T‐cell sensitivity (Li et al ., 2007), although its mechanistic action remains unclear. We found that miR‐181a‐3p was coexpressed with and predicted to target three immune response genes, namely CXCL16 , RAB27A, and SPON2 .…”

Section: Discussionmentioning

confidence: 99%

Age‐associated microRNA expression in human peripheral blood is associated with all‐cause mortality and age‐related traits

et al. 2017

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SummaryRecent studies provide evidence of correlations of DNA methylation and expression of protein‐coding genes with human aging. The relations of microRNA expression with age and age‐related clinical outcomes have not been characterized thoroughly. We explored associations of age with whole‐blood microRNA expression in 5221 adults and identified 127 microRNAs that were differentially expressed by age at P < 3.3 × 10−4 (Bonferroni‐corrected). Most microRNAs were underexpressed in older individuals. Integrative analysis of microRNA and mRNA expression revealed changes in age‐associated mRNA expression possibly driven by age‐associated microRNAs in pathways that involve RNA processing, translation, and immune function. We fitted a linear model to predict ‘microRNA age’ that incorporated expression levels of 80 microRNAs. MicroRNA age correlated modestly with predicted age from DNA methylation (r = 0.3) and mRNA expression (r = 0.2), suggesting that microRNA age may complement mRNA and epigenetic age prediction models. We used the difference between microRNA age and chronological age as a biomarker of accelerated aging (Δage) and found that Δage was associated with all‐cause mortality (hazards ratio 1.1 per year difference, P = 4.2 × 10−5 adjusted for sex and chronological age). Additionally, Δage was associated with coronary heart disease, hypertension, blood pressure, and glucose levels. In conclusion, we constructed a microRNA age prediction model based on whole‐blood microRNA expression profiling. Age‐associated microRNAs and their targets have potential utility to detect accelerated aging and to predict risks for age‐related diseases.

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“…Our group and others have reported that MSCs could regulate the differentiation, maturation and functions of immune cells, such as T cells, B cells, macrophages, dendritic cells and NK cells [9][10][11][12]. The immunoregulatory activities of MSCs are in turn enhanced by inflammatory cytokines such as interferon-c (IFN-c) and interleukin-1b (IL-1b) derived from activated immune cells [13,14].…”

Section: Introductionmentioning

confidence: 99%

MiR‐30a attenuates immunosuppressive functions of IL‐1β‐elicited mesenchymal stem cells via targeting TAB3

Ding

Miao

et al. 2015

FEBS Letters

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a b s t r a c tMesenchymal stem cells (MSCs) possess the ability to modulate the immune response, and their abnormalities are related to several diseases. We previously reported that miR-30a expression significantly increased in the maternal-fetal interface during preeclampsia (PE), but the effects of miR-30a on the immunoregulatory characteristics of MSCs are unclear. In this study, we determined that miR-30a over-expression inhibited the IL-1b-elicited activation of the nuclear factor jB (NF-jB) and JNK signaling pathways and the production of IL-6, cyclooxygenase 2 (COX2) and IL-8 by targeting transforming growth factor-b-activated kinase 1 binding protein 3 (TAB3) in MSCs. Moreover, the over-expression of miR-30a also impaired MSCs' anti-inflammatory effects on macrophages. These data demonstrated that miR-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE.

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MicroRNA‐181a Regulates Local Immune Balance by Inhibiting Proliferation and Immunosuppressive Properties of Mesenchymal Stem Cells

Cited by 88 publications

References 73 publications

MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-β signaling

MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-β signaling

Age‐associated microRNA expression in human peripheral blood is associated with all‐cause mortality and age‐related traits

MiR‐30a attenuates immunosuppressive functions of IL‐1β‐elicited mesenchymal stem cells via targeting TAB3

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MicroRNA‐181a Regulates Local Immune Balance by Inhibiting Proliferation and Immunosuppressive Properties of Mesenchymal Stem Cells

Cited by 88 publications

References 73 publications

MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-&beta; signaling

MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-&beta; signaling

Age‐associated microRNA expression in human peripheral blood is associated with all‐cause mortality and age‐related traits

MiR‐30a attenuates immunosuppressive functions of IL‐1β‐elicited mesenchymal stem cells via targeting TAB3

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MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-β signaling

MicroRNA-181a-5p enhances cell proliferation in medullary thymic epithelial cells via regulating TGF-β signaling