RGD Reference Report - MicroRNA-152 modulates the canonical Wnt pathway activation by targeting DNA methyltransferase 1 in arthritic rat model. - Rat Genome Database

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MicroRNA-152 modulates the canonical Wnt pathway activation by targeting DNA methyltransferase 1 in arthritic rat model.

Authors: Miao, Cheng-Gui  Yang, Ying-Ying  He, Xu  Huang, Cheng  Huang, Yan  Qin, Dan  Du, Chuan-Lai  Li, Jun 
Citation: Miao CG, etal., Biochimie. 2014 Nov;106:149-56. doi: 10.1016/j.biochi.2014.08.016. Epub 2014 Sep 4.
RGD ID: 21066343
Pubmed: PMID:25194984   (View Abstract at PubMed)
DOI: DOI:10.1016/j.biochi.2014.08.016   (Journal Full-text)

Rheumatoid arthritis (RA) is an autoimmune and progressive systemic disease of unknown etiology. Research shows that fibroblast-like synoviocytes (FLS) participate in the cartilage erosion, synovial hyperplasia, inflammatory cytokine secretion and suggests that fibroblast-like synoviocytes (FLS) display a crucial role in RA pathogenesis. Recent studies have suggested the role of the Wnt signaling pathway in the pathogenesis of RA. In previous study, we identified that increased methyl-CpG-binding protein 2 (MeCP2) reduced the secreted frizzled-related protein 4 (SFRP4) expression in FLS in Arthritic rat model and the DNA methyltransferase (DNMT) inhibitor 5-Aza-2'-deoxycytidine (5-azadC) could induce the SFRP4 expression, indicating that DNMT has a key role in the differential expression of SFRP4. MicroRNAs (MiRNAs), which are small non-coding RNAs, are involved in diverse biological functions, regulation of gene expression, pathogenesis of autoimmune disease and carcinogenesis. In light of the directly down-regulation of miR-152 on DNMT1 expression by targeting the 3' untranslated regions of its transcript in nickel sulfide (NiS)-transformed human bronchial epithelial cells, we investigated whether miR-152 is aberrantly expressed and targets DNMT1 in FLS in Arthritic rat model. Our results demonstrated that the expression of miR-152 was specifically down-regulated in Arthritic rat model, whereas up-regulation of miR-152 in FLS resulted in a marked reduction of DNMT1 expression. Further experiments revealed that increased miR-152 indirectly up-regulated the SFRP4 expression, a negative regulator of WNT signaling pathway, by targeting the DNMT1. Moreover, activation of miR-152 expression in FLS could inhibit the canonical Wnt pathway activation and result in a significant decrease of FLS proliferation. MiR-152 and DNA methylation may provide molecular mechanisms for the activation of canonical Wnt pathway in RA. Combination of miR-152 and DNMT1 may be a promising treatment strategy for RA patients in which SFRP4 is inactivated.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MIR152HumanExperimental Arthritis  ISOMir152 (Rattus norvegicus)miRNA:decreased exression:synovial membrane of synovial jointRGD 
Mir152MouseExperimental Arthritis  ISOMir152 (Rattus norvegicus)miRNA:decreased exression:synovial membrane of synovial jointRGD 
Mir152RatExperimental Arthritis  IEP miRNA:decreased exression:synovial membrane of synovial jointRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Mir152Ratnegative regulation of fibroblast proliferation  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir152  (microRNA 152)

Genes (Mus musculus)
Mir152  (microRNA 152)

Genes (Homo sapiens)
MIR152  (microRNA 152)


Additional Information