LINC00520 targeting miR-27b-3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway.
Acute Kidney Injury
/ genetics
Animals
Cell Line
Cell Proliferation
/ genetics
Gene Expression Regulation
/ genetics
Gene Knockdown Techniques
Humans
MicroRNAs
/ genetics
Oncogene Protein v-akt
/ genetics
Oncostatin M Receptor beta Subunit
/ genetics
Phosphatidylinositol 3-Kinases
/ genetics
RNA, Long Noncoding
/ genetics
Rats
Signal Transduction
/ genetics
LINC00520
OSMR
PI3K-AKT
acute kidney injury
miR-27b-3p
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
24
10
2018
accepted:
11
12
2018
pubmed:
27
1
2019
medline:
27
5
2020
entrez:
27
1
2019
Statut:
ppublish
Résumé
Acute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy. Bioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real-time PCR (qRT-PCR) and western blot. Dual-luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI. LINC00520, miR-27b-3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI. Overexpression of LINC00520 contributes to the aggravation of AKI by targeting miR-27b-3p/ OSMR.
Sections du résumé
BACKGROUND
Acute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy.
METHODS
Bioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real-time PCR (qRT-PCR) and western blot. Dual-luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI.
RESULTS
LINC00520, miR-27b-3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI.
CONCLUSION
Overexpression of LINC00520 contributes to the aggravation of AKI by targeting miR-27b-3p/ OSMR.
Substances chimiques
MIRN27 microRNA, human
0
MicroRNAs
0
OSMR protein, human
0
Oncostatin M Receptor beta Subunit
0
RNA, Long Noncoding
0
Oncogene Protein v-akt
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
14221-14233Informations de copyright
© 2019 Wiley Periodicals, Inc.