Mir-133 microRNA precursor family

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mir-133 microRNA precursor family
RF00446.jpg
Predicted secondary structure and sequence conservation of mir-133
Identifiers
Symbolmir-133
Rfam RF00446
miRBase MI0000450
miRBase family MIPF0000029
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO GO:0035195 GO:0035068
SO SO:0001244
PDB structures PDBe

mir-133 is a type of non-coding RNA called a microRNA that was first experimentally characterised in mice. [1] Homologues have since been discovered in several other species including invertebrates such as the fruitfly Drosophila melanogaster . Each species often encodes multiple microRNAs with identical or similar mature sequence. For example, in the human genome there are three known miR-133 genes: miR-133a-1, miR-133a-2 and miR-133b found on chromosomes 18, 20 and 6 respectively. The mature sequence is excised from the 3' arm of the hairpin. miR-133 is expressed in muscle tissue and appears to repress the expression of non-muscle genes. [2]

Contents

Regulation

It is proposed that Insulin activates the translocation of SREBP-1c (BHLH) active form from the endoplasmic reticulum (ER) to the nucleus and, concomitantly, induces SREPB-1c expression via PI3K signaling pathway. SREBP-1c mediates MEF2C downregulation through a mechanism that remains to be determined. As a consequence of lower MEF2C binding on their enhancer region, the transcription of miR-1 and miR-133a is reduced, leading to decreased levels of their mature forms in muscle, after insulin treatment. Altered activation of PI3K and SREBP-1c may explain the defective regulation of miR-1 and miR-133a expression in response to insulin in muscle of type 2 diabetic patients. [3]

Targets of miR-133

microRNAs act by lowering the expression of genes by binding to target sites in the 3' UTR of the mRNAs. Luo et al.. demonstrated that the HCN2 K+ channel gene contains a target of miR-133. [4] Yin et al.. showed that the Mps1 kinase gene in zebrafish is a target. [5] Boutz et al.. showed that nPTB (neuronal polypyrimidine tract-binding protein) is a target and likely contains two target sites for miR-133. [6] Xiao et al.. show that ether-a-go-go related gene (ERG) a K+ channel is a target of miR-133. [7]

miR-133 directly and negatively regulates NFATc4. [8] [9]

RhoA expression is negatively regulated by miR-133a in bronchial smooth muscles (BSM)and miR-133a downregulation causes an upregulation of RhoA, resulting in an augmentation of contraction and BSM hyperresponsiveness. [10]

BMP2 downregulates multiple mIRs, of which one, miR-133, directly inhibits Runx2, an early BMP response gene essential for bone formation. Although miR-133 is known to promote MEF-2-dependent myogenesis, it also inhibits Runx2-mediated osteogenesis. BMP2 controls bone cell determination by inducing miRNAs that target muscle genes but mainly by down-regulating multiple miRNAs that constitute an osteogenic program, thereby releasing from inhibition pathway components required for cell lineage commitment establish a mechanism for BMP morphogens to selectively induce a tissue-specific phenotype and suppress alternative lineages. [11]

Nicotine activates α7-nAChR and downregulates the levels of miR-133 and miR-590 leading to significant upregulation of expression of TGF-β1 and TGF-βRII at the protein level establishing miR-133 and miR-590 as repressors of TGF-β1 and TGF-βRII. [12]

miR-133 enhances myoblast proliferation by repressing serum response factor (SRF) [13]

mIR-133 suppresses SP1 expression [14]

In rats, miR-133b is expressed in retinal dopaminergicamacrine cell, and this expression is significantly increased during early stage during retinal degeneration. This overexpression leads to downregulation of the transcription factor PITX3. [15] miR-133a is down regulated in diabetic cardiomyopathy. [16]

miR-133 suppresses Prdm16 expression in skeletal muscle stem cells (satellite cells), which controls myogenic vs. brown adipogenic lineage determination in these cells. [17]

Related Research Articles

<span class="mw-page-title-main">Sterol regulatory element-binding protein</span> Protein family

Sterol regulatory element-binding proteins (SREBPs) are transcription factors that bind to the sterol regulatory element DNA sequence TCACNCCAC. Mammalian SREBPs are encoded by the genes SREBF1 and SREBF2. SREBPs belong to the basic-helix-loop-helix leucine zipper class of transcription factors. Unactivated SREBPs are attached to the nuclear envelope and endoplasmic reticulum membranes. In cells with low levels of sterols, SREBPs are cleaved to a water-soluble N-terminal domain that is translocated to the nucleus. These activated SREBPs then bind to specific sterol regulatory element DNA sequences, thus upregulating the synthesis of enzymes involved in sterol biosynthesis. Sterols in turn inhibit the cleavage of SREBPs and therefore synthesis of additional sterols is reduced through a negative feed back loop.

mir-1 microRNA precursor family

The miR-1 microRNA precursor is a small micro RNA that regulates its target protein's expression in the cell. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give products at ~22 nucleotides. In this case the mature sequence comes from the 3' arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. In humans there are two distinct microRNAs that share an identical mature sequence, and these are called miR-1-1 and miR-1-2.

<span class="mw-page-title-main">Sterol regulatory element-binding protein 1</span> Protein-coding gene in the species Homo sapiens

Sterol regulatory element-binding transcription factor 1 (SREBF1) also known as sterol regulatory element-binding protein 1 (SREBP-1) is a protein that in humans is encoded by the SREBF1 gene.

mIRN21 Non-coding RNA in the species Homo sapiens

microRNA 21 also known as hsa-mir-21 or miRNA21 is a mammalian microRNA that is encoded by the MIR21 gene.

mir-127

mir-127 microRNA is a short non-coding RNA molecule with interesting overlapping gene structure. miR-127 functions to regulate the expression levels of genes involved in lung development, placental formation and apoptosis. Aberrant expression of miR-127 has been linked to different cancers.

mir-145 Non-coding RNA in the species Homo sapiens

In molecular biology, mir-145 microRNA is a short RNA molecule that in humans is encoded by the MIR145 gene. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

mir-200

In molecular biology, the miR-200 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by binding and cleaving mRNAs or inhibiting translation. The miR-200 family contains miR-200a, miR-200b, miR-200c, miR-141, and miR-429. There is growing evidence to suggest that miR-200 microRNAs are involved in cancer metastasis.

mir-223 Mir-223

In molecular biology MicroRNA-223 (miR-223) is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. miR-223 is a hematopoietic specific microRNA with crucial functions in myeloid lineage development. It plays an essential role in promoting granulocytic differentiation while also being associated with the suppression of erythrocytic differentiation. miR-223 is commonly repressed in hepatocellular carcinoma and leukemia. Higher expression levels of miRNA-223 are associated with extranodal marginal-zone lymphoma of mucosa-associated lymphoid tissue of the stomach and recurrent ovarian cancer. In some cancers the microRNA-223 down-regulation is correlated with higher tumor burden, disease aggressiveness, and poor prognostic factors. MicroRNA-223 is also associated with rheumatoid arthritis, sepsis, type 2 diabetes, and hepatic ischemia.

mir-221 microRNA

In molecular biology, mir-221 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

miR-138

miR-138 is a family of microRNA precursors found in animals, including humans. MicroRNAs are typically transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product. The excised region or, mature product, of the miR-138 precursor is the microRNA mir-138.

miR-33 Non-coding RNA in the species Homo sapiens

miR-33 is a family of microRNA precursors, which are processed by the Dicer enzyme to give mature microRNAs. miR-33 is found in several animal species, including humans. In some species there is a single member of this family which gives the mature product mir-33. In humans there are two members of this family called mir-33a and mir-33b, which are located in intronic regions within two protein-coding genes for Sterol regulatory element-binding proteins respectively.

In recent years it has become apparent that the environment and underlying mechanisms affect gene expression and the genome outside of the central dogma of biology. It has been found that many epigenetic mechanisms are involved in the regulation and expression of genes such as DNA methylation and chromatin remodeling. These epigenetic mechanisms are believed to be a contributing factor to pathological diseases such as type 2 diabetes. An understanding of the epigenome of Diabetes patients may help to elucidate otherwise hidden causes of this disease.

In molecular biology mir-365 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology mir-370 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. This microRNA, mir-370-3p, has been shown to play a role in heart failure. The upregulation of mir-370-3p in the sinus node leads to downregulation of the pacemaker ion channel, HCN4, and thus downregulation of the corresponding ionic current, which causes sinus bradycardia.

In molecular biology mir-153 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology mir-590 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology mir-872 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology mir-938 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

<span class="mw-page-title-main">MIR34A</span> Non-coding RNA in the species Homo sapiens

MicroRNA 34a (miR-34a) is a MicroRNA that in humans is encoded by the MIR34A gene.

References

  1. ↑ Lagos-Quintana M, Rauhut R, Yalcin A, Meyer J, Lendeckel W, Tuschl T (Apr 2002). "Identification of tissue-specific microRNAs from mouse". Current Biology. 12 (9): 735–9. doi:10.1016/S0960-9822(02)00809-6. hdl: 11858/00-001M-0000-0010-94EF-7 . PMID   12007417. S2CID   7901788.
  2. ↑ Ivey KN, Muth A, Arnold J, King FW, Yeh RF, Fish JE, Hsiao EC, Schwartz RJ, Conklin BR, Bernstein HS, Srivastava D (Mar 2008). "MicroRNA regulation of cell lineages in mouse and human embryonic stem cells". Cell Stem Cell. 2 (3): 219–29. doi:10.1016/j.stem.2008.01.016. PMC   2293325 . PMID   18371447.
  3. ↑ Granjon A, Gustin MP, Rieusset J, Lefai E, Meugnier E, Güller I, Cerutti C, Paultre C, Disse E, Rabasa-Lhoret R, Laville M, Vidal H, Rome S (Nov 2009). "The microRNA signature in response to insulin reveals its implication in the transcriptional action of insulin in human skeletal muscle and the role of a sterol regulatory element-binding protein-1c/myocyte enhancer factor 2C pathway". Diabetes. 58 (11): 2555–64. doi:10.2337/db09-0165. PMC   2768160 . PMID   19720801.
  4. ↑ Luo X, Lin H, Pan Z, Xiao J, Zhang Y, Lu Y, Yang B, Wang Z (Jul 2008). "Down-regulation of miR-1/miR-133 contributes to re-expression of pacemaker channel genes HCN2 and HCN4 in hypertrophic heart". The Journal of Biological Chemistry. 283 (29): 20045–52. doi: 10.1074/jbc.M801035200 . PMC   3151107 . PMID   18458081.
  5. ↑ Yin VP, Thomson JM, Thummel R, Hyde DR, Hammond SM, Poss KD (Mar 2008). "Fgf-dependent depletion of microRNA-133 promotes appendage regeneration in zebrafish". Genes & Development. 22 (6): 728–33. doi:10.1101/gad.1641808. PMC   2275425 . PMID   18347091.
  6. ↑ Boutz PL, Chawla G, Stoilov P, Black DL (Jan 2007). "MicroRNAs regulate the expression of the alternative splicing factor nPTB during muscle development". Genes & Development. 21 (1): 71–84. doi:10.1101/gad.1500707. PMC   1759902 . PMID   17210790.
  7. ↑ Xiao J, Luo X, Lin H, Zhang Y, Lu Y, Wang N, Zhang Y, Yang B, Wang Z (Apr 2007). "MicroRNA miR-133 represses HERG K+ channel expression contributing to QT prolongation in diabetic hearts". The Journal of Biological Chemistry. 282 (17): 12363–7. doi: 10.1074/jbc.C700015200 . PMC   3151106 . PMID   17344217.
  8. ↑ Li Q, Lin X, Yang X, Chang J (May 2010). "NFATc4 is negatively regulated in miR-133a-mediated cardiomyocyte hypertrophic repression". American Journal of Physiology. Heart and Circulatory Physiology. 298 (5): H1340-7. doi:10.1152/ajpheart.00592.2009. PMC   3774484 . PMID   20173049.
  9. ↑ Dong DL, Chen C, Huo R, Wang N, Li Z, Tu YJ, Hu JT, Chu X, Huang W, Yang BF (Apr 2010). "Reciprocal repression between microRNA-133 and calcineurin regulates cardiac hypertrophy: a novel mechanism for progressive cardiac hypertrophy". Hypertension. 55 (4): 946–52. doi: 10.1161/HYPERTENSIONAHA.109.139519 . PMID   20177001.
  10. ↑ Chiba Y, Misawa M (2010). "MicroRNAs and their therapeutic potential for human diseases: MiR-133a and bronchial smooth muscle hyperresponsiveness in asthma". Journal of Pharmacological Sciences. 114 (3): 264–8. doi: 10.1254/jphs.10R10FM . PMID   20953121.
  11. ↑ Li Z, Hassan MQ, Volinia S, van Wijnen AJ, Stein JL, Croce CM, Lian JB, Stein GS (Sep 2008). "A microRNA signature for a BMP2-induced osteoblast lineage commitment program". Proceedings of the National Academy of Sciences of the United States of America. 105 (37): 13906–11. doi: 10.1073/pnas.0804438105 . PMC   2544552 . PMID   18784367.
  12. ↑ Shan H, Zhang Y, Lu Y, Zhang Y, Pan Z, Cai B, Wang N, Li X, Feng T, Hong Y, Yang B (2009). "Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines". Cardiovasc. Res. 83 (3): 465–72. doi: 10.1093/cvr/cvp130 . PMID   19398468.
  13. ↑ Chen JF, Mandel EM, Thomson JM, Wu Q, Callis TE, Hammond SM, Conlon FL, Wang DZ (2006). "The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation". Nat. Genet. 38 (2): 228–33. doi:10.1038/ng1725. PMC   2538576 . PMID   16380711.
  14. ↑ Torella D (2011). "MicroRNA-133 Controls Vascular Smooth Muscle Cell Phenotypic Switch In Vitro and Vascular Remodeling In Vivo". Circulation Research. 109 (8): 880–893. doi: 10.1161/CIRCRESAHA.111.240150 . hdl: 2434/225968 . PMID   21852550.
  15. ↑ Li Y, Li C, Chen Z, He J, Tao Z, Yin ZQ (Mar 2012). "A microRNA, mir133b, suppresses melanopsin expression mediated by failure dopaminergic amacrine cells in RCS rats". Cellular Signalling. 24 (3): 685–98. doi:10.1016/j.cellsig.2011.10.017. PMID   22101014.
  16. ↑ Chavali V, Tyagi SC, Mishra PK (2014). "Differential expression of dicer, miRNAs, and inflammatory markers in diabetic Ins2+/- Akita hearts". Cell Biochem. Biophys. 68 (1): 25–35. doi:10.1007/s12013-013-9679-4. PMC   4085798 . PMID   23797610.
  17. ↑ Yin H, Pasut A, Soleimani VD, Bentzinger CF, Antoun G, Thorn S, Seale P, Fernando P, van Ijcken W, Grosveld F, Dekemp RA, Boushel R, Harper ME, Rudnicki MA (Feb 2013). "MicroRNA-133 controls brown adipose determination in skeletal muscle satellite cells by targeting Prdm16". Cell Metabolism. 17 (2): 210–24. doi:10.1016/j.cmet.2013.01.004. PMC   3641657 . PMID   23395168.

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