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MiR-155 is a microRNA that in humans is encoded by the MIR155 host gene or MIR155HG. MiR-155 plays an important role in various physiological and pathological processes. Exogenous molecular control in vivo of miR-155 expression may inhibit malignant growth, viral infections, and attenuate the progression of cardiovascular diseases.
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MiR-155 is a microRNA that in humans is encoded by the MIR155 host gene or MIR155HG.[1] MiR-155 plays an important role in various physiological and pathological processes.[2][3][4][5] Exogenous molecular control in vivo of miR-155 expression may inhibit malignant growth,[6][7] viral infections,[8][9] and attenuate the progression of cardiovascular diseases.[10]
[edit] MIR155HG overview
The MIR155HG was initially identified as a gene that was transcriptionally activated by promoter insertion at a common retroviral integration site in B-cell lymphomas and was formerly called BIC (B-cell Integration Cluster).[11] It was latter found that the MIR155HG was composed of three exons that span a 13 kb region within human chromosome 21 (Hsa21 band q21.3) (see Figure 1).[12] The MIR155HG is transcribed by RNA polymerase II and the resulting ~1,500 nucleotide RNA is capped and polyadenylated. The 23 nucleotide single-stranded miR-155, which is harbored in exon 3, is subsequently processed from the parent RNA molecule.[13]
Figure 1. Schematic representation of the MIR155HG (accession # NC_000021). This gene spans 13024 bp, is comprised of three exons, and encodes a 1500 bp non-coding primary-miRNA (pri-miRNA) (accession # NR_001458). The location of the pre-mir-155 is denoted by the orange box.
[edit] miR-155 biogenesis
The MIR155HG RNA transcript does not contain a long open reading frame (ORF), however, it does include an imperfectly base-paired stem loop that is highly conserved across species.[12] This non-coding RNA (ncRNA) is now defined as a primary-miRNA (pri-miRNA).[12] Once miR-155 pri-miRNA is transcribed, this transcript is cleaved by the nuclear microprocessor complex, of which the core components are the RNase III type endonuclease Drosha and the DiGeorge critical region 8 (DGCR8) protein,[14][15] to produce a 65 nucleotide stem-loop precursor miRNA (pre-mir-155) (see Figure 2).
Figure 2. The sequence of the pre-mir-155 stem loop that is matured from the pri-miRNA transcript. The mature miR-155 (miR-155-5p) sequence is shown in green and mature miR-155* (miR-155-3p) sequence is shown in red.
Following export from the nucleus by exportin-5, pre-mir-155 molecules are cleaved near the terminal loop by Dicer resulting in RNA duplexes of ~22nucleotides.[14][15] Following Dicer cleavage, an Argonaute (Ago) protein binds to the short RNA duplexes, forming the core of a multi-subunit complex called the RNA-induced silencing complex (RISC).[16] In a manner similar to siRNA duplexes, one of the two strands, the “passenger miRNA” (miR-155*), is released and degraded while the other strand, designated the “guide strand” or “mature miRNA” (miR-155), is retained within the RISC.[16]
Recent data suggest that both arms of the pre-miRNA hairpin can give rise to mature miRNAs.[17][18] Due to the increasing number of examples where two functional mature miRNAs are processed from opposite arms of the same pre-miRNA, pre-mir-155 products are now denoted with the suffix -5p (from the 5′ arm) (e.g. miR-155-5p) and -3p (from the 3′ arm) (e.g. miR-155-3p) following their name (see Figure 3).[19]
Figure 3. The mature miR-155 (miR-155-5p) sequence is shown in green and mature miR-155* (miR-155-3p) sequence is shown in red.
Once miR-155-5p/-3p is assembled into the RISC, these molecules subsequently recognize their target messenger RNA (mRNA) by base pairing interactions between nucleotides 2 and 8 of miR-155 (the seed region) and complementary nucleotides predominantly in the 3'-untranslated region (3'-UTR) of mRNAs (see Figure 4).[20] Finally, with the miR-155-5p/-3p acting as an adaptor for the RISC, complex-bound mRNAs are subjected to translational repression (i.e. inhibition of translation initiation) and/or degradation following deadenylation.[16]
Figure 4. Complementary base-pairing between miR-155-5p and the human angiotensin II type 1 receptor (hAT1R) mRNA binding site located 70–90 base pairs downstream from the stop codon. The requisite "seed sequence" base-pairing is denoted by the bold dashes.
[edit] Phylogenetic characteristics
Early phylogenetic analyses demonstrated that the sequence of pre-mir-155 and miR-155-5p was highly conserved between human, mouse, and chicken.[12] Recent annotated sequencing data found that 22 different organisms including, mammals, amphibians, birds, reptiles, sea squirts, and sea lampreys, express a highly conserved miR-155-5p.[2] Currently much less sequence data is available regarding miR-155-3p, therefore, it is not clear how conserved this miRNA is across species.[3]
[edit] Expression Patterns
Northern blot analysis found that miR-155 pri-miRNA was abundantly expressed in the human spleen and thymus and detectable in the liver, lung, and kidney.[12] Subsequently, polymerase chain reaction (PCR) experiments demonstrated that miR-155-5p was detectable in all human tissues investigated.[21] Sequence analysis of small RNA clone libraries comparing miRNA expression to all other organ systems examined established that miR-155-5p was one of five miRNAs (i.e. miR-142, miR-144, miR-150, miR-155, and miR-223) that was highly specific for hematopoietic cells including B-cells, T-cells, monocytes and granulocytes.[22] Together these results suggest that miR-155-5p is expressed in a number of tissues and cell types and, therefore, may play a critical role in a wide variety of biological processes, including hematopoiesis [2][3][4]
Although very few studies have investigated the expression levels of miR-155-3p, Landgraf et al.[22] established that expression levels of this miRNA was very low in hematopoietic cells. Additionally, PCR analyses found that while miR-155-3p was detectable in a number of human tissues the expression levels of this miRNA were 20-200 fold less when compared to miR-155-5p levels.[23] Even though the function of miR-155-3p has been largely ignored, several studies now suggest that, in some cases (astrocytes and plasmacytoid dendritic cells), both miR-155-5p and -3p can be functionally matured from pre-mir-155.[24][25]
[edit] Targets
Bioinformatic analysis utilizing TargetScan 6.2 (release date June, 2012) [4] revealed at least 4,174 putative human miR-155-5p mRNA targets exist, with a total of 918 conserved sites (i.e. between mouse and human) and 4,249 poorly conserved sites (i.e. human only).[20][26] Although the TargetScan 6.2 algorithm cannot be utilized to determine the miR-155-3p putative targets, one would speculate that this miRNA may also potentially regulate the expression of thousands of mRNA targets. It is important to note that a number of predicted mRNA targets turn out to be false while others are overlooked entirely.
A comprehensive list of miR-155-5p/mRNA targets that were experimentally authenticated by both the demonstration of endogenous transcript regulation by miR-155-5p and validation of the miR-155-5p seed sequence through a reporter assay was recently assembled.[27] This list was comprised of 140 genes and included regulatory proteins for myelopoiesis and leukemogenesis (e.g. AICDA, ETS1, JARID2, SPI1, etc.), inflammation (e.g. BACH1, FADD, IKBKE, INPP5D, MYD88, RIPK1, SPI1, SOCS, etc.) and known tumor suppressors (e.g. CEBPβ, IL17RB, PCCD4, TCF12, ZNF652, etc.).[27]
[edit] Physiological roles
[edit] Hematopoiesis
In support that this miRNA plays a critical role in hematopoiesis, mice deficient in pre-mir-155 showed clear defects in lymphocyte development and generation of B- and T-cell responses in vivo, and an impaired antigen-presenting function of dendritic cells.[28][29][30] Further, it was established that regulatory T-cells (Tregs) development required miR-155-5p but that it was dispensable for Treg proliferation or survival in the periphery.[31] Additionally, miR-155-5p was shown to play an important role in Treg homeostasis and overall survival by directly targeting SOCS1, a negative regulator for IL-2 signaling.[32] Since miR-155-5p was found to be highly expressed in CD34(+) human hematopoietic stem-progenitor cells (HSPCs), it was hypothesized that this miRNA may hold these cells at an early stem-progenitor stage, blocking their differentiation into a more mature cell (i.e. granulocytic/monocytic/erythroid/megakaryocytic/B-lymphoid).[33] This premise was corroborated when pre-mir-155 transduced HSPCs generated 5-fold fewer myeloid and 3-fold fewer erythroid colonies.[33] Additionally, Hu et al.[34] demonstrated that the homeobox protein, HOXA9, regulated miR-155-5p expression in myeloid cells and that this miRNA played a functional role in hematopoiesis. These investigators found that forced expression of miR-155-5p in bone marrow cells resulted in a ~50% decrease in SPI1 (i.e. PU.1),[34] a transcription factor and an important regulator of myelopoiesis[35] and a validated target of this miRNA.[30] Finally, it was established that in vitro differentiation of purified human erythroid progenitor cells resulted in a progressive decrease of miR-155-5p expression in mature red cells.[36] Taken together, these results strongly suggest that miR-155-5p is an essential molecule in the control of several aspects of hematopoiesis including erythropoiesis, lymphopoiesis, and myelopoiesis.
[edit] Activity and phenotypes
The hallmark of miR-155 activities is that they transcend to and fro within protective roles to normal physiological functions to disease associated manifestations. It is estimated to participate in cascades associated with cardiovascular diseases and hypertension, and was also found to be implicated in immunity, genomic instability, cell differentiation, inflammation, virus associated infections and cancer.
Protective roles of miR-155 may arise in response to its action on silencing genes thereby regulating their expression time, mutations in miR-155 target site deny it the optimal access necessary to bring about gene silencing, leading to over abundance of delinquent activities that may go malignant, for example, miR-155 role as a protective agent against predisposition to B Cell associated malignancies is emphasized by maintaining the balance of Activation-Induced Cytidine Deaminase (AID) enzyme. MiR-155 mediates regulation of AID abundance and expression time upon immunological cues however, mutations in the target on AID mRNA result in its unresponsiveness to miR-155 silencing and lead to unbridled expression of its protein causing wild immature B-lymphocyte surges and AID-mediated chromosomal translocations.[3][4]
[edit] Clinical significance
[edit] Cardiopulmonary disease and hypertension
Transfection of miR-155 into human primary lung fibroblasts reduces the endogenous expression of the angiotensin II receptor AT1R protein. Furthermore, AT1R is involved in cardiovascular and blood pressure ailments by controlling angiotension II. Defective miR-155 function could be implicated in hypertension and cardiovascular diseases if the cis-regulatory site on 3` UTR of AT1R (miR-155 target site) was affected due to a SNP polymorphism in AT1R itself. This mutation is disruptive of miR-155 targeting and thus preventive of AT1R expression down-regulation.[3] In low blood pressure over-expression of miR-155 correlates with the impairment of AT1R activity.[2]
[edit] Immunity
miR-155 is highly involved in immunity by playing key roles in modulating humoral and innate cell-mediated immune responses, for example, In miR-155 deficient mice, immunological-memory is impaired; making it fall prey to repetitive bouts of invasions by the same pathogen (Rodriguez et al. 2007),maturation and specificity of miR-155-deficient B-lymphocytes are impaired since the process relies on AID enzyme which has a miR-155 target in its 3' UTR end.[3][4] The phenotypic consequences involving deficiency of miR-155 in mice show later in life where the animals develop lung and intestinal lesions.[2]
Activated B and T cells show increased miR-155 expression, the same goes for macrophages and dendritic cells of the immune system. MiR-155 is crucial for proper lymphocyte development and maturation. Details of various manifestations of miR-155 levels and involvement in activities that ascertain optimal immune responses have been the subject of many researches:
[edit] Reduction of IgG1
Defective T and B cells as well as markedly decreased IgG1 responses were observed in miR-155-deficient mice, IgG1 is reduced whereas the expression of the IgM immunoglobulin remains normal in these mice. The abnormality in IgG1 levels maybe explained by an important target for miR-155 in B cells, the protein-encoding mRNA for the transcriptional regulator Pu.1-protein, elevation of Pu.1 protein predisposes defective IgG1 production. In addition to Pu.1, there are nearly 60 other differentially elevated genes in miR-155 deficient B cells, further inspection revealed possible miR-155 target sites in the 3' UTR regions in these genes.[4]
[edit] Predisposition to lymphocyte malignancies
Mature receptors affinity and specificity of lymphocytes to pathogenic agents underlie proper immune responses, optimal miR-155 coordination is required for manufacturing of normal B lymphocytes and production of high-affinity antibodies and memory cells, this has been evidenced by comparisons of miR-155 expression patterns in normal and abnormal B cells revealing a miR-155 role in differentiation. Were miR-155 expression abnormally elevated; pre-B cell lymphomas formed.[4] By Understanding how the process of B cell development takes place we can clearly see the significance of miR-155 in this regard; selection of competent B cells takes place in the germinal center where they are trained to differentiate body cells vs. foreign antigens, they compete for antigen recognition and for T cell help, in this fashion of selective pressure those B Cells that demonstrated high-affinity receptors and cooperation with T cells (affinity maturation) are recruited and deployed to the bone marrow or become memory B cells, apoptotic termination takes place for those B Cells failing the competition. Immature B cells which are miR-155 deficient evade apoptosis as a result of elevated Bcl-2 protein levels; a protein that was found to be involved in B Cell malignancies and to be controlled by miR-155.[4]
[edit] Inflammation
Inflammatory responses to triggers such as TNF-α involve macrophages with components that include miR-155. miR-155 is overexpressed in atopic dermatitis and contributes to chronic skin inflammation by increasing the proliferative response of T(H) cells through the downregulation of CTLA-4.[37] In Autoimmune disorders such as Rheumatoid Arthritis miR-155 showed higher expression in patients' tissues and synovial fibroblasts.[2]
[edit] DNA viruses
In DNA viruses, miRNAs were experimentally verified, miRNAs in viruses are encoded by dsDNAs,[3] examples of such viruses include herpesviruses such as Humans-Epstein-Barr Virus (EBV) and adenoviruses,[2] another virus expressing miR-155-like miRNA in chickens is the oncogenic MDV-1 whose non-oncogenic relative MDV-2 does not, this suggests implication of miR-155 in lymphomagenesis.[3] Viruses can exploit host miRNAs to the degree that they use host miRNAs to encode for viral clones for example: MiR-k12-11 in Kaposi's-sarcoma-associated Herpesvirus has a target specificity region orthologous to that of miR-155's; mimicking the action of miR-155[2][3] and, sharing targets with it, thus it can be thought to suppress miR-155 accessibility to its targets by competition and this in effect downregulates expression of genes playing roles in cellular growth and apoptosis in a manner that defies regulations by miR-155.[2] EBV modulates host miR-155. EBV-infected cells have increased expression of miR-155 thereby disturbing equilibrium of expression for genes regulating transcription in those cells.[2][3]
[edit] Cancer
Over-silencing by miR-155 may result in triggering oncogenic cascades that begin by apoptotic resistance, The pro-apoptotic Tumour Protein-53-induced-nuclear-protein1 (TP53INP1) is silenced by miR-155, over-expression of miR-155 leads to decreased levels of TP53INP1 in pancreatic ductal adenocarcinomas and possibly in other epithelial cancers where TP53INP1 activity is lost thereby resulting in apoptosis evasion and uncontrolled bouts of growth.[3]
Inactivation of DNA Mismatch Repair (MMR) as identified by elevation of mutation rates is the cause of Lynch Syndrome (LS), also known as hereditary nonpolyposis colorectal cancer (HNPCC), down-regulation of MMR controlling protein is carried out by over-expression of miR-155, MMR is controlled by a group of highly conserved proteins, reduced activity of these proteins results in elevated levels of mutations in the phenotype triggering a march towards developing this type of cancer.[38]
Other types of tumors in which miR-155 over-expression was reported include: thyroid carcinoma, breast cancer, colon cancer, cervical cancer, and lung cancer, where distinct miR-155 expression profiles quantification can potentially serve as signals for tumor detection and evaluation of prognosis outcome.[2]
[edit] Images
[edit] References
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[edit] Further reading
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