RGD Reference Report - MicroRNA-21 contributes to high glucose-induced fibrosis in peritoneal mesothelial cells in rat models by activation of the Ras-MAPK signaling pathway via Sprouty-1. - Rat Genome Database

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MicroRNA-21 contributes to high glucose-induced fibrosis in peritoneal mesothelial cells in rat models by activation of the Ras-MAPK signaling pathway via Sprouty-1.

Authors: Gao, Qing  Xu, Lin  Yang, Qian  Guan, Tian-Jun 
Citation: Gao Q, etal., J Cell Physiol. 2019 May;234(5):5915-5925. doi: 10.1002/jcp.26941. Epub 2018 Dec 4.
RGD ID: 40925948
Pubmed: PMID:30515805   (View Abstract at PubMed)
DOI: DOI:10.1002/jcp.26941   (Journal Full-text)

Peritoneal fibrosis remains to be one of the most severe causes of failure in continuous peritoneal dialysis. The current study cultured peritoneal mesothelial cells in high glucose to stimulate the environment of peritoneal fibrosis model in rats, and investigate whether microRNA-21 (miR-21) targeting Sprouty-1 affects high glucose-induced fibrosis in peritoneal mesothelial cells via the rennin angiotensin system (Ras)-mitogen-activated protein kinase (MAPK) signaling pathway, as well as potential mechanisms. Peritoneal tissues in fibrosis rats were collected to extract peritoneal mesothelial cells, which, after in vitro culture, were transfected with a series of mimic or inhibitor of miR-21, or the small interfering RNA (siRNA) against Sprouty-1. Reverse-transcription quantitative polymerase chain reaction and western blot analyses were performed to determine the levels of related genes or proteins. MTT assay and flow cytometry were conducted to observe the cell viability and cell apoptosis of peritoneal mesothelial cells. Dual-luciferase reporter gene assay revealed that Sprouty-1 is the target gene of miR-21. Peritoneal fibrosis manifested with elevated miR-21, extracellular-signal-regulated kinase (ERK), c-Jun NH2-terminal protein kinase (JNK), RAS and p38MAPK but reduced Sprouty-1. Cells transfected with miR-21 mimic exhibited decreased Sprouty-1 expressions, but increased levels of ERK, JNK, RAS, and p38MAPK. As for cellular process, miR-21 mimic or siRNA against Sprouty-1 exposure reduced cell viability, which resulted in more cells arrested at the G1 stage, and induced apoptosis. In contrast, miR-21 inhibitor exposure was observed to have induced effects on peritoneal mesothelial cells. These key findings provide evidence that miR-21 inhibits Sprouty-1 to promote the progression of fibrosis in peritoneal mesothelial cells by activating the Ras-MAPK signaling pathway.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Peritoneal Fibrosis  ISOMir21 (Rattus norvegicus)40925948; 40925948RNA:increased expression:peritoneal fluid and tissueRGD 
Peritoneal Fibrosis  IEP 40925948RNA:increased expression:peritoneal fluid and tissueRGD 
Peritoneal Fibrosis  ISOSpry1 (Rattus norvegicus)40925948; 40925948mRNA more ...RGD 
Peritoneal Fibrosis  IEP 40925948mRNA more ...RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of apoptotic process  IMP 40925948 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir21  (microRNA 21)
Spry1  (sprouty RTK signaling antagonist 1)

Genes (Mus musculus)
Mir21a  (microRNA 21a)
Spry1  (sprouty RTK signaling antagonist 1)

Genes (Homo sapiens)
MIR21  (microRNA 21)
SPRY1  (sprouty RTK signaling antagonist 1)


Additional Information