RGD Reference Report - MiR-542-3p drives renal fibrosis by targeting AGO1 in vivo and in vitro. - Rat Genome Database

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MiR-542-3p drives renal fibrosis by targeting AGO1 in vivo and in vitro.

Authors: Li, Jue  Bao, Haijiao  Zhang, Kaiyue  Yang, Xiaotao  Liu, Xuemei  Li, Pengfei  Li, Qingli  Chen, Weiwen 
Citation: Li J, etal., Life Sci. 2020 Aug 15;255:117845. doi: 10.1016/j.lfs.2020.117845. Epub 2020 May 26.
RGD ID: 401900731
Pubmed: PMID:32470449   (View Abstract at PubMed)
DOI: DOI:10.1016/j.lfs.2020.117845   (Journal Full-text)


AIMS: Renal fibrosis is the typical manifestation of progressive kidney disease and causes a severe threat to human health. Surging evidence has illustrated that miRNA plays a core role in the genesis and development of kidney fibrosis. MiR-542-3p has been testified to function as a facilitator in hepatic stellate cell activation and fibrosis. The purpose of study is to investigate the potential of miR-542-3p in renal tubulointerstitial fibrosis.
MATERIALS AND METHODS: In this study, to establish renal fibrosis model in vivo and in vitro, we first conducted unilateral ureteral obstruction (UUO) on rats and high glucose (HG) treatment on the HK-2 cells. Histological and western blot analyses were utilized for assessment of renal fibrosis model. Luciferase reporter assay was carried out to explore the regulatory mechanism underlying miR-542-3p in renal fibrosis.
KEY FINDINGS: MiR-542-3p was found to be highly expressed in renal fibrosis. Functional experiments revealed that overexpression of miR-542-3p accelerated the deterioration of kidney fibrosis and inhibition of miR-542-3p led to the opposite result. Through the aid of bioinformatics tool, the speculated miR-542-3p binding sites were uncovered in the 3'UTR of argonaute RISC component 1 (AGO1). Mechanism study elucidated that AGO1 was a direct target of miR-542-3p. Lastly, our findings suggested that miR-542-3p played a promoting role in renal fibrosis via repression of AGO1.
SIGNIFICANCE: We justified that miR-542-3p induced kidney fibrogenesis both in vivo and in vitro through targeting AGO1, unveiling that miR-542-3p might be a promising option for the treatment of patients with renal fibrosis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MIR542Humanrenal fibrosis  ISOMir542 (Rattus norvegicus)RNA:increased expression:kidneyRGD 
Mir542Mouserenal fibrosis  ISOMir542 (Rattus norvegicus)RNA:increased expression:kidneyRGD 
Mir542Ratrenal fibrosis  IEP RNA:increased expression:kidneyRGD 
MIR542HumanTubulointerstitial Fibrosis exacerbatesISOMir542 (Rattus norvegicus) RGD 
Mir542MouseTubulointerstitial Fibrosis exacerbatesISOMir542 (Rattus norvegicus) RGD 
Mir542RatTubulointerstitial Fibrosis exacerbatesIDA  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Mir542Ratrenal tubule atrophy amelioratesIMP  RGD 
Objects Annotated

Genes (Rattus norvegicus)
Mir542  (microRNA 542)

Genes (Mus musculus)
Mir542  (microRNA 542)

Genes (Homo sapiens)
MIR542  (microRNA 542)


Additional Information