Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-019-40747-8
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Funding
- Carl Gottschalk career development award (American Society of Nephrology)
- Pilot Discovery grant (Center for Genomic Medicine, MUSC)
- Genomics Shared Resource, Hollings Cancer Center, Medical University of South Carolina [P30CA138313]
- American Society of Nephrology
- Center for Genomic Medicine, SCTR
- Augusta University
- JSPS KAKENHI [15H04594, 16K15047, 18H02348, 15K18784, 18K05996]
- Grants-in-Aid for Scientific Research [18K05996, 16K15047, 15K18784, 18H02348, 15H04594] Funding Source: KAKEN
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Because exosomes have gained attention as a source of biomarkers, we investigated if miRNAs in exosomes (exo-miRs) can report the disease progression of organ injury. Using rat renal ischemia-reperfusion injury (IRI) as a model of acute kidney injury (AKI), we determined temporally-released exo-miRs in urine during IRI and found that these exo-miRs could reliably mirror the progression of AKI. From the longitudinal measurements of miRNA expression in kidney and urine, we found that release of exo-miRs was a regulated sorting process. In the injury state, miR-16, miR-24, and miR-200c were increased in the urine. Interestingly, expression of target mRNAs of these exo-miRs was significantly altered in renal medulla. Next, in the early recovery state, exo-miRs (miR-9a, miR-141, miR-200a, miR-200c, miR-429), which share Zeb1/2 as a common target mRNA, were upregulated together, indicating that they reflect TGF-beta-associated renal fibrosis. Finally, release of exo-miRs (miR-125a, miR-351) was regulated by TGF-beta 1 and was able to differentiate the sham and IRI even after the injured kidneys were recovered. Altogether, these data indicate that exo-miRs released in renal IRI are associated with TGF-beta signaling. Temporal release of exo-miRs which share targets might be a regulatory mechanism to control the progression of AKI.
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