Involvement of neutrophil gelatinase-associated lipocalin and osteopontin in renal tubular regeneration and interstitial fibrosis after cisplatin-induced renal failure

Kashiwagi, Emi; Tonomura, Yutaka; Kondo, Chiaki; Masuno, Koichi; Fujisawa, Kae; Tsuchiya, Naho; Matsushima, Shuuichi; Torii, Mikinori; Takasu, Nobuo; Izawa, Takeshi; Kuwamura, Mitsuru; Yamate, Jyoji

doi:10.1016/j.etp.2014.04.007

Cited by 34 publications

(23 citation statements)

References 24 publications

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“…Recent studies correlated Lcn2 and Fg-b expression with AKI development in mice. 28,29 Overexpression of these markers of renal injury was reduced by wild-type MSCs and EVs but not MSC-Dsh and EV-Dsh. Inefficiency of Drosha-knockdown cells and EVs in inducing renal repair was observed at not only morphologic level but also, functional levels as indicated by the persistence of elevated BUN levels.…”

Section: Discussionmentioning

confidence: 98%

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AKI Recovery Induced by Mesenchymal Stromal Cell-Derived Extracellular Vesicles Carrying MicroRNAs

Collino

Bruno²,

Incarnato

et al. 2015

Journal of the American Society of Nephrology

220

227

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Phenotypic changes induced by extracellular vesicles have been implicated in mesenchymal stromal cellpromoted recovery of AKI. MicroRNAs are potential candidates for cell reprogramming toward a proregenerative phenotype. The aim of this study was to evaluate whether microRNA deregulation inhibits the regenerative potential of mesenchymal stromal cells and derived extracellular vesicles in a model of glycerol-induced AKI in severe combined immunodeficient mice. We generated mesenchymal stromal cells depleted of Drosha to alter microRNA expression. Drosha-knockdown cells produced extracellular vesicles that did not differ from those of wild-type cells in quantity, surface molecule expression, and internalization within renal tubular epithelial cells. However, these vesicles showed global downregulation of microRNAs. Whereas wild-type mesenchymal stromal cells and derived vesicles administered intravenously induced morphologic and functional recovery in AKI, the Drosha-knockdown counterparts were ineffective. RNA sequencing analysis showed that kidney genes deregulated after injury were restored by treatment with mesenchymal stromal cells and derived vesicles but not with Drosha-knockdown cells and vesicles. Gene ontology analysis showed in AKI an association of downregulated genes with fatty acid metabolism and upregulated genes with inflammation, matrix-receptor interaction, and cell adhesion molecules. These alterations reverted after treatment with wild-type mesenchymal stromal cells and extracellular vesicles but not after treatment with the Drosha-knockdown counterparts. In conclusion, microRNA depletion in mesenchymal stromal cells and extracellular vesicles significantly reduced their intrinsic regenerative potential in AKI, suggesting a critical role of microRNAs in recovery after AKI.

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Section: Discussionmentioning

confidence: 98%

“…Kidneys from untreated AKI mice showed elevated levels of transcripts coding for markers of tubular damage, such as lipocalin 2 (Lcn2) 28 and fibrinogen (Fg) subunits, 29 as detected by RNA-Seq analysis. In healthy mice, no expression of Lcn2 was observed.…”

Section: Effect Of Drosha Knockdown On the Expression Of Markers Of Kmentioning

confidence: 99%

AKI Recovery Induced by Mesenchymal Stromal Cell-Derived Extracellular Vesicles Carrying MicroRNAs

Collino

Bruno²,

Incarnato

et al. 2015

Journal of the American Society of Nephrology

220

227

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show abstract

“…OPN is used as a biomarker for renal injury; its expression is related to the extent of renal damage (Kashiwagi et al, 2014;Wadey et al, 2014). OPN immune-reactivity may be seen in renal tubules, particularly in the loop of Henley, in normal rats (Wadey et al, 2014); however, the reactivity of OPN was faint and limited in the present control rats.…”

Section: Immunohistochemistry For Opn and Bmp-6 In Renal Fibrosismentioning

confidence: 93%

Participation of bone morphogenetic protein (BMP)-6 and osteopontin in cisplatin (CDDP)-induced rat renal fibrosis

Yano

Golbar

Izawa

et al. 2015

Experimental and Toxicologic Pathology

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“…It is proposed that, in addition to bacteriostasis, NGAL may by inhibiting apoptosis and enhancing cellular proliferation/differentiation [14,15] also have a reparatory role in injured epithelial tubular cells.…”

Section: Introductionmentioning

confidence: 99%

“…Urinary NGAL assessed early after transplantation and long-term graft prognosis.Graft survival after one year between donor with serum NGAL ≥214 ng/ml vs. donors with NGAL b214 ng/ml eGFR: estimated glomerular filtration rate, AUC/ROC: area under receiver operating characteristic curve, Se: Sensitivity, Sp: Specificity [4][5][6][7][8][9][10][11][12][13][14][15][16][17]. ng/ml compared to 59 [IQR 33-136] ng/ml).…”

mentioning

confidence: 99%

Neutrophil gelatinase-associated lipocalin in kidney transplantation: A review

Ramirez‐Sandoval

Herrington

Morales‐Buenrostro

2015

Transplantation Reviews

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Involvement of neutrophil gelatinase-associated lipocalin and osteopontin in renal tubular regeneration and interstitial fibrosis after cisplatin-induced renal failure

Cited by 34 publications

References 24 publications

AKI Recovery Induced by Mesenchymal Stromal Cell-Derived Extracellular Vesicles Carrying MicroRNAs

AKI Recovery Induced by Mesenchymal Stromal Cell-Derived Extracellular Vesicles Carrying MicroRNAs

Participation of bone morphogenetic protein (BMP)-6 and osteopontin in cisplatin (CDDP)-induced rat renal fibrosis

Neutrophil gelatinase-associated lipocalin in kidney transplantation: A review

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