Altered microRNAs in STHdhQ111/HdhQ111 cells: miR-146a targets TBP

Sinha, Mithun; Ghose, Jayeeta; Das, Eashita; Bhattarcharyya, Nitai P.

doi:10.1016/j.bbrc.2010.05.007

Cited by 64 publications

(80 citation statements)

References 39 publications

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“…miR-146a is an important regulator in both innate and adaptive immune response. Its expression is upregulated upon TLR agonist stimulation, proinflammatory cytokine stimulation, viral infection, and viral component stimulation (25,28,29). In macrophages, TLR2, TLR4, and TLR5 agonists activated miR-146a expression, whereas TLR3, TLR7, or TLR9 agonists failed to do so (25).…”

Section: Discussionmentioning

confidence: 99%

“…Consistently, we showed that miR-146a could target Notch1 to repress IL-12p70 production in CpG-ODNstimulated DCs. miRNAs function mainly through repressing their target mRNAs, and the known miR-146a targets, such as IRAK1, IRAK2, TRAF6, and TBP, seem to be unrelated to IL-12p70 production (25,28,29). Hence, targeting of Notch1 by miR146a may be responsible for the miR-146a-mediated repression of IL-12p70 production in CpG-ODN-stimulated DCs.…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs function mainly through repressing their target mRNAs, and the known miR-146a targets, such as IRAK1, IRAK2, TRAF6, and TBP, seem to be unrelated to IL-12p70 production (25,28,29). We searched for new possible targets of miR-146a through TargetScan prediction (http://www.…”

Section: Cd11b Represses Cpg-odn-triggered Notch1 Expression In Dcs Vmentioning

confidence: 99%

“…Among them, miR-146a plays key roles in innate immunity, inflammatory response, and viral infection. Both TLR activation and inflammatory stimulation can lead to the upregulation of miR-146a, which, in turn, negatively regulates innate immunity by repressing its targets, such as IRAK1, IRAK2, TNFR-associated factor (TRAF)6, and TATA-binding protein (TBP) (25,28,29). The induction of miR-146a is reported to be dependent on NF-kB activation (25), but the precise regulatory mechanism remains unclear.…”

mentioning

confidence: 99%

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Integrin CD11b Negatively Regulates TLR9-Triggered Dendritic Cell Cross-Priming by Upregulating microRNA-146a

Bai

Qian

et al. 2012

The Journal of Immunology

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Dendritic cells (DCs) play critical roles in cross-priming to induce the CTL response against infection; however, the molecular mechanisms for the regulation of DC cross-priming need to be investigated further, which may help to improve the potency of DC vaccines through engineering modifications. Our previous studies showed that β2 integrin CD11b could control TLR-triggered NK cell cytotoxicity and macrophage inflammatory responses. CD11b is also abundantly expressed in DCs, but it is unknown whether CD11b participates in the regulation of DC cross-priming for the CTL response. Also, because microRNAs (miRNAs) are important regulators of the immune response, it remains unclear whether miRNAs are regulated by CD11b in DCs. In this study, we showed that CD11b deficiency upregulated TLR9-triggered, but not TLR4-triggered, IL-12p70 production in DCs, subsequently promoting DC cross-priming of the CTL response. Further experiments showed that CD11b selectively promoted TLR9-triggered miR-146a upregulation in DCs by sustaining late-phase NF-κB activation. Additionally, Notch1, a known positive regulator of IL-12p70 production in DCs, was confirmed to be directly targeted by miR-146a. miR-146a upregulation and Notch1 repression were determined to be responsible for the reduced IL-12p70 production in TLR9-triggered wild-type DCs compared with that in CD11b-deficient DCs. Therefore, CD11b and downstream miR-146a may be new negative regulators for DC cross-priming by suppressing Notch1 expression and IL-12p70 production. Our data indicate a new mechanism for the regulation of DC cross-priming through integrins and miRNAs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Cd11b Represses Cpg-odn-triggered Notch1 Expression In Dcs Vmentioning

confidence: 99%

mentioning

confidence: 99%

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Integrin CD11b Negatively Regulates TLR9-Triggered Dendritic Cell Cross-Priming by Upregulating microRNA-146a

Bai

Qian

et al. 2012

The Journal of Immunology

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“…Methods used for detection of miRNA expression using stem loop specific primers and expression of protein coding genes using gene specific primers were similar to that has been published earlier [15,16]. List of primers for cloning pre-miR-432, 3 0 -UTR of the target genes and gene expression studies and their ensemble ID are shown in Supplementary Table S2A.…”

Section: Quantitative Real-time Reverse Transcription Pcr (Qrt-pcr) Fmentioning

confidence: 99%

MicroRNA‐432 contributes to dopamine cocktail and retinoic acid induced differentiation of human neuroblastoma cells by targeting NESTIN and RCOR1 genes

Das

Bhattacharyya

2014

FEBS Letters

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Edited by Tamas Dalmay Keywords:MicroRNA-432 NESTIN RCOR1 MECP2 Neurite outgrowth SH-SY5Y cells a b s t r a c t MicroRNA (miRNA) regulates expression of protein coding genes and has been implicated in diverse cellular processes including neuronal differentiation, cell growth and death. To identify the role of miRNA in neuronal differentiation, SH-SY5Y and IMR-32 cells were treated with dopamine cocktail and retinoic acid to induce differentiation. Detection of miRNAs in differentiated cells revealed that expression of many miRNAs was altered significantly. Among the altered miRNAs, human brain expressed miR-432 induced neurite projections, arrested cells in G0-G1, reduced cell proliferation and could significantly repress NESTIN/NES, RCOR1/COREST and MECP2. Our results reveal that miR-432 regulate neuronal differentiation of human neuroblastoma cells.

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Overview of Huntington's Disease Models: Neuropathological, Molecular, and Behavioral Differences

Rangel‐Barajas

Rebec

2018

CP Neuroscience

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Transgenic mouse models of Huntington's disease (HD), a neurodegenerative condition caused by a single gene mutation, have been transformative in their ability to reveal the molecular processes and pathophysiological mechanisms underlying the HD behavioral phenotype. Three model categories have been generated depending on the genetic context in which the mutation is expressed: truncated, full-length, and knock-in. No single model, however, broadly replicates the behavioral symptoms and massive neuronal loss that occur in human patients. The disparity between model and patient requires careful consideration of what each model has to offer when testing potential treatments. Although the translation of animal data to the clinic has been limited, each model can make unique contributions toward an improved understanding of the neurobehavioral underpinnings of HD. Thus, conclusions based on data obtained from more than one model are likely to have the most success in the search for new treatment targets. © 2018 by John Wiley & Sons, Inc.

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Altered microRNAs in STHdhQ111/HdhQ111 cells: miR-146a targets TBP

Cited by 64 publications

References 39 publications

Integrin CD11b Negatively Regulates TLR9-Triggered Dendritic Cell Cross-Priming by Upregulating microRNA-146a

Integrin CD11b Negatively Regulates TLR9-Triggered Dendritic Cell Cross-Priming by Upregulating microRNA-146a

MicroRNA‐432 contributes to dopamine cocktail and retinoic acid induced differentiation of human neuroblastoma cells by targeting NESTIN and RCOR1 genes

Overview of Huntington's Disease Models: Neuropathological, Molecular, and Behavioral Differences

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