MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha

Li, Yingke; Fan, Xiaoping; He, Xing‐Ying; Sun, Haijing; Zou, Zui; Yuan, Hongbin; Xu, Haitao; Wang, Chengcai; Shi, Xueyin

doi:10.1038/cmi.2012.35

Cited by 55 publications

(47 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…70 Recently, we have demonstrated that miR-466l can directly bind to the 39-UTR of IFN-a and reduce its expression during VSV infection. 111 There is mounting evidence that type I IFN can manipulate miRNA expression. A recent study that used an in-depth miRNome analysis of resting and IFN-a-activated human natural killer cells revealed that IFN-a activation suppressed two abundantly expressed miRNAs, miR-378 and miR-30e, which allowed the translation of cytolytic mRNAs, resulting in augmented natural killer cell cytotoxicity.…”

Section: Mirna-mediated Regulation Of Rig-i Signaling Pathway and Virmentioning

confidence: 99%

MicroRNAs in the regulation of TLR and RIG-I pathways

2012

Self Cite

View full text Add to dashboard Cite

The innate immune system recognizes invading pathogens through germline-encoded pattern recognition receptors (PRRs), which elicit innate antimicrobial and inflammatory responses and initiate adaptive immunity to control or eliminate infection. Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I) are the key innate immune PRRs and are tightly regulated by elaborate mechanisms to ensure a beneficial outcome in response to foreign invaders. Although much of the focus in the literature has been on the study of protein regulators of inflammation, microRNAs (miRNAs) have emerged as important controllers of certain features of the inflammatory process. Several miRNAs are induced by TLR and RIG-I activation in myeloid cells and act as feedback regulators of TLR and RIG-I signaling. In this review, we comprehensively discuss the recent understanding of how miRNA networks respond to TLR and RIG-I signaling and their role in the initiation and termination of inflammatory responses. Increasing evidence also indicates that both virus-encoded miRNAs and cellular miRNAs have important functions in viral replication and host anti-viral immunity.

show abstract

Section: Mirna-mediated Regulation Of Rig-i Signaling Pathway and Virmentioning

confidence: 99%

MicroRNAs in the regulation of TLR and RIG-I pathways

2012

Self Cite

View full text Add to dashboard Cite

show abstract

“…although the iFN type i response is also regulated, either indirectly by other prrs like Tlr-2 and Tlr-4 (mir-19, let7e or mir-200 family) or directly by iFN-α mrNa suppression (mir-466l) (ref. 96 ), all pathogenetic modes of mirs regulation of iFN type i expression require further study. Whereas iFN type i has been established as the main contributor to sle pathogenesis 97 , it is not surprising that the expression of mir-146a in pBmcs of sle patients negatively correlates with disease activity and severity of renal involvement 94,98 .…”

Section: Innate Immunity and Mirs And Slementioning

confidence: 99%

MicroRNAs in the key events of systemic lupus erythematosus pathogenesis

Hušáková¹

2016

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

View full text Add to dashboard Cite

Background. Small non-coding RNA molecules (miRs) are involved in immune cell maturation and function and might influence immunopathological processes of systemic lupus erythematosus (SLE) pathogenesis. Methods and Results. This paper presents the results of a literature search for publications dealing with the relationship between miRs and pathological factors related to SLE such as genetic background, immune dysregulation and gender-associated differences participating in SLE development. In SLE, distinct miRs are differentially expressed in SLE cells of innate and adaptive immunity. The miR-146a and miR-155 genes, among others, interfere with intracellular signalling pathways downstream of toll-like receptors 7 and 9 (TLR-7, TLR-9) and influences interferon (IFN)-type I synthesis in plasmacytoid dendritic cells. In T and B cells, miR-126, miR-21, miR-146a, miR-155, miR-1246 and others might influence gene expression by epigenetic modifications, support abnormal cytosine release, differentiation of cell subsets, B cell hyperactivity and autoantibody production. Besides, estrogen might up-and downregulate immunologically active miRs, which are potential mediators of hormonal influences in SLE development. Moreover, SLE genetic basis included some polymorphisms of the miR-146a gene, which varies across populations. Conclusion. Distinct miRs are differentially expressed in both SLE mice models and human patients and promote autoimmune features of immune processes. MiRs are important molecules modulating susceptibility to SLE as well as its onset, clinical diversity and progression.

show abstract

“…32 Downregulation of miR-338 has been associated with progression and severity of human gastric, colorectal, and hepatocellular carcinomas; however, the potential role of miR-338 in our model of TEVG stenosis is unclear. [33][34][35] On the other hand, miR-466 may regulate components of the innate immune system (IL-10 and IFN-a), 36,37 which we have demonstrated to be a critical determinant of TEVG patency, 38 and is therefore a potential target for further study.…”

Section: Discussionmentioning

confidence: 99%

Novel Association of miR-451 with the Incidence of TEVG Stenosis in a Murine Model

Hibino

Best

Engle

et al. 2016

Tissue Engineering Part A

View full text Add to dashboard Cite

The development of a tissue-engineered vascular graft (TEVG) holds great promise for advancing the field of cardiac surgery. Despite the successful translation of this technology, previous reports identify the primary mode of graft failure as stenosis secondary to intimal hyperplasia. MicroRNAs (miRNAs) regulate gene expression by interfering with mRNA function and recent research has suggested miRNA as a potential therapeutic target. The role of miRNAs in TEVGs during neotissue formation is currently unknown. In this study, we investigated if miRNAs regulate the inhibition of graft stenosis. Biodegradable PGA-P(LA/CL) scaffolds were implanted as inferior vena cava interposition grafts in a murine model (n = 14). Mice were sacrificed 14 days following implantation and TEVGs were harvested for histological analysis and miRNA profiling using Affymetrix miRNA arrays. Graft diameters were measured histologically, and the largest grafts (patent group) and smallest grafts (stenosed group) were profiled (n = 4 for each group). Cell population in each graft was analyzed with immunohistochemistry using antismooth muscle actin (SMA) and antimacrophage (F4/ 80) antibodies. The graft diameter was significantly greater in the patent group (0.63 -0.06 mm) than in the stenosed group (0.17 -0.06 mm) ( p < 0.01). Cell proliferation was significantly greater in the stenosed grafts than in patent grafts ( p < 0. MiRNA array of 1416 genes showed that in stenosed grafts, mir-451, mir-338, and mir-466 were downregulated and mir-154 was upregulated. Mir-451 exhibited the greatest difference in expression between stenosed and patent grafts by -3.1-fold. Significant negative correlation was found between the expression of mir-451 and cell proliferation (SMA: r = -0.86, p = 0.003; F4/80: r = -0.89, p = 0.001). Our data, along with previous evidence that mir-451 regulates tumor suppressor genes, suggest that downregulation of mir-451 promotes acute proliferation of macrophages and smooth muscle cells, thereby inducing TEVG stenosis. Adequate expression of mir-451 may be critical for improving TEVG patency.

show abstract

MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha

Cited by 55 publications

References 40 publications

MicroRNAs in the regulation of TLR and RIG-I pathways

MicroRNAs in the regulation of TLR and RIG-I pathways

MicroRNAs in the key events of systemic lupus erythematosus pathogenesis

Novel Association of miR-451 with the Incidence of TEVG Stenosis in a Murine Model

Contact Info

Product

Resources

About