SVF
Level C· Early Human ResearchProspective Study

Renal Vein Levels of MicroRNA-26a Are Lower in the Poststenotic Kidney.

Zhu XY., Ebrahimi B., Eirin A., Woollard JR., Tang H., Jordan KL.

Prospective Study with a reported sample of 7 on Acute Kidney Injury, published in J Am Soc Nephrol (2015) — summary generated from the PubMed abstract.

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Prospective Study
Journal
J Am Soc Nephrol (2015)
Country
United States
Reported sample size
7
PMID
25270070
DOI
10.1681/ASN.2014030248

Abstract (original English)

MicroRNA-26a (miR-26a) is a post-transcriptional regulator that inhibits cellular differentiation and apoptosis. Renal vascular disease (RVD) induces ischemic injury characterized by tubular cell apoptosis and interstitial fibrosis. We hypothesized that miR-26a levels are reduced in the poststenotic kidney and that kidney repair achieved by adipose tissue-derived mesenchymal stem cells (ad-MSCs) is associated with restored miR-26a levels. Renal function and renal miR-26a levels were assessed in pigs with RVD not treated (n=7) or 4 weeks after intrarenal infusion of ad-MSC (2.5×10(5) cells/kg; n=6), patients with RVD (n=12) or essential hypertension (n=12), and healthy volunteers (n=12). In addition, the direct effect of miR-26a on apoptosis was evaluated in a renal tubular cell culture. Compared with healthy control kidneys, swine and human poststenotic kidneys had 45.5±4.3% and 90.0±3.5% lower levels of miR-26a, respectively, which in pigs, localized to the proximal tubules. In pigs, ad-MSC delivery restored tubular miR-26a expression, attenuated tubular apoptosis and interstitial fibrosis, and improved renal function and tubular oxygen-dependent function. In vitro, miR-26a inhibition induced proximal tubular cell apoptosis and upregulated proapoptotic protein expression, which were both rescued by ad-MSC. In conclusion, decreased tubular miR-26a expression in the poststenotic

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples, often without a control group.

How we grade evidence
Acute Kidney InjuryAgedAnalysis of VarianceAnimalsBiopsy, NeedleCase-Control StudiesCells, CulturedDisease Models, AnimalFemaleHumans
Systemic / IVAcute Kidney Injury
View on PubMedDOI

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