miR-221 and miR-155 regulate human dendritic cell development, apoptosis, and IL-12 production through targeting of p27kip1, KPC1, and SOCS-1

Lu, Changming; Huang, Xin; Zhang, Xiaoxiao; Roensch, Kristin; Cao, Qing; Nakayama, Keiichi I.; Blazar, Bruce R.; Zeng, Yan; Zhou, Xianzheng

doi:10.1182/blood-2010-12-322503

Cited by 251 publications

(245 citation statements)

References 48 publications

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“…Similarly for what was described for regulation of IL-6 by miR-155 (Ceppi et al, 2009;O'Connell et al, 2010;Dunand-Sauthier et al, 2011), a positive role for miR-155 in mouse moDC maturation is contrasted by a reported negative role of miR-155 for maturation of human moDC, at least based on DC-Sign expression (Martinez-Nunez et al, 2009). Maturation from monocytes into moDCs was also found to be correlated with decreased miR-211 (Lu et al, 2011a). Maturation of human CD14 + moDCs was also found recently to be inhibited by miR-146a .…”

Section: Maturation From Monocytes Into Modcssupporting

confidence: 58%

“…Similarly, inhibition of miR-511 and miR-99b resulted in reduced DC-SIGN levels (Tserel et al, 2011). As being a versatile miRNA, miR-155 is also positively involved in maturation of mouse moDCs (Dunand-Sauthier et al, 2011;Lu et al, 2011a). Transcription factor c-Fos as a target of miR-155 was negatively for moDC maturation (Dunand-Sauthier et al, 2011).…”

Section: Maturation From Monocytes Into Modcsmentioning

confidence: 99%

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Functional regulation of monocyte-derived dendritic cells by microRNAs

Zhan¹,

Wu²

2012

Protein Cell

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Section: Maturation From Monocytes Into Modcssupporting

confidence: 58%

Section: Maturation From Monocytes Into Modcsmentioning

confidence: 99%

Functional regulation of monocyte-derived dendritic cells by microRNAs

Zhan¹,

Wu²

2012

Protein Cell

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“…miR150 is required for the crosspresentation capacity of Langerhans cells (skinresident DCs) [45] . In addition, miR29b, miR 29c [46] , miR126 [47] , miR146a [40,48] , miR155, and miR221 [49] have been shown to regulate DC apoptosis and cytokine production.…”

Section: Mirnas and Dcsmentioning

confidence: 99%

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Zhang

2016

WJG

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Inflammatory bowel disease (IBD) is characterized by chronic relapsing inflammatory disorders of the gastrointestinal tract, and includes two major phenotypes: ulcerative colitis and Crohn's disease. The pathogenesis of IBD is not fully understood as of yet. It is believed that IBD results from complicated interactions between environmental factors, genetic predisposition, and immune disorders. miRNAs are a class of small non-coding RNAs that can regulate gene expression by targeting the 3′-untranslated region of specific mRNAs for degradation or translational inhibition. miRNAs are considered to play crucial regulatory roles in many biologic processes, such as immune cellular differentiation, proliferation, and apoptosis, and maintenance of immune homeostasis. Recently, aberrant expression of miRNAs was revealed to play an important role in autoimmune diseases, including IBD. In this review, we discuss the current understanding of how miRNAs regulate autoimmunity and inflammation by affecting the differentiation, maturation, and function of various immune cells. In particular, we focus on describing specific miRNA expression profiles in tissues and peripheral blood that may be associated with the pathogenesis of IBD. In addition, we summarize the opportunities for utilizing miRNAs as new biomarkers and as potential therapeutic targets in IBD.

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“…miRNA-155 regulates cell processes, including cell survival, growth, and chemosensitivity (29) and dendritic development and apoptosis (30). The relative expression levels of the target gene were evaluated using the most stable reference gene (miR-101a and U87) vs. the least reference stable gene (snoRNA).…”

Section: Assessment Of Validitymentioning

confidence: 99%

Identification of suitable reference genes for BDV-infected primary rat hippocampal neurons

Mao

Zhang

Guo

et al. 2016

Molecular Medicine Reports

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Abstract. Borna disease virus (BDV) is a neurotropic RNA virus that infects the limbic system of mammals and results in behavioral disorders. The hippocampus is a core region in the limbic system, which contributes to memory and learning and is important in the regulation of emotion. However, no validated microRNA housekeeping genes have yet been identified in BDV-infected rat primary hippocampal neurons. Proper normalization is key in accurate miRNA expression analysis. The present study used reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to evaluate the expression stability of 10 commonly used reference genes 5S, U6, E2 small nucleolar RNA (snoRNA), in BDV-infected rat hippocampal neurons and non-infected controls across 12 days post-infection. The data was analyzed by four statistical algorithms: geNorm, NormFinder, BestKeeper, and the comparative Δ-Ct method. Subsequently, the most suitable reference genes (miR-101a and U87) and the least suitable (snoRNA) were determined by the RankAggreg package. miR-155 was selected as a standard by which to evaluate the most and least suitable reference genes. When normalized to the most stable reference gene there were significant differences between the two groups. However, when the data were normalized to the less stably expressed gene, the results were not significant. miR-101a was recommended as a suitable reference gene for BDV-infected rat primary hippocampal neurons.

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miR-221 and miR-155 regulate human dendritic cell development, apoptosis, and IL-12 production through targeting of p27kip1, KPC1, and SOCS-1

Cited by 251 publications

References 48 publications

Functional regulation of monocyte-derived dendritic cells by microRNAs

Functional regulation of monocyte-derived dendritic cells by microRNAs

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Identification of suitable reference genes for BDV-infected primary rat hippocampal neurons

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