Therapeutic use of human renal progenitor cells for kidney regeneration

Bussolati, Benedetta; Camussi, Giovanni

doi:10.1038/nrneph.2015.126

Cited by 54 publications

(45 citation statements)

References 100 publications

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“…The mechanism involved in the repair after human renal cell administration can be ascribed to integration into the renal tubules and in parallel to a paracrine mechanism based on reno-protective molecules8. We here observed a persistence of CD133 + cells up to 30 days within the tissue that may possibly underline a transient integration within renal structures as well as a paracrine mechanism.…”

Section: Discussionsupporting

confidence: 49%

“…A number of studies showed a protective effect of adult human renal cells in tissue protection and functional repair in AKI, including CD133 expressing cells8. An effect on the reduction of early tissue fibrosis (up to day 14) was also shown using CD133 + embryonic renal cells29.…”

Section: Discussionmentioning

confidence: 97%

“…New experimental strategies to promote a correct restitutio ad integrum , i. e. the restoration of the original tissue integrity after AKI are therefore needed, possibly including treatment with therapeutic cell sources or reno-protective bioproducts8. The population of CD133 + renal progenitor cells (CD133 + cells) isolated from human tissue has been previously used as a therapeutic cell source in murine models of AKI91011.…”

mentioning

confidence: 99%

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Human CD133+ Renal Progenitor Cells Induce Erythropoietin Production and Limit Fibrosis After Acute Tubular Injury

Aggarwal

Grange

Iampietro

et al. 2016

Sci Rep

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Persistent alterations of the renal tissue due to maladaptive repair characterize the outcome of acute kidney injury (AKI), despite a clinical recovery. Acute damage may also limit the renal production of erythropoietin, with impairment of the hemopoietic response to ischemia and possible lack of its reno-protective action. We aimed to evaluate the effect of a cell therapy using human CD133+ renal progenitor cells on maladaptive repair and fibrosis following AKI in a model of glycerol-induced rhabdomyolysis. In parallel, we evaluated the effect of CD133+ cells on erythropoietin production. Administration of CD133+ cells promoted the restoration of the renal tissue, limiting the presence of markers of injury and pro-inflammatory molecules. In addition, it promoted angiogenesis and protected against fibrosis up to day 60. No effect of dermal fibroblasts was observed. Treatment with CD133+ cells, but not with PBS or fibroblasts, limited anemia and increased erythropoietin levels both in renal tissue and in circulation. Finally, CD133+ cells contributed to the local production of erythropoietin, as observed by detection of circulating human erythropoietin. CD133+ cells appear therefore an effective source for cell repair, able to restore renal functions, including erythropoietin release, and to limit long term maldifferentiation and fibrosis.

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Section: Discussionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

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Human CD133+ Renal Progenitor Cells Induce Erythropoietin Production and Limit Fibrosis After Acute Tubular Injury

Aggarwal

Grange

Iampietro

et al. 2016

Sci Rep

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“…Akut böbrek hastalığı veya subklinik greft rejeksiyonu, hastaları kronik böbrek hastalığına götürür. Kronik böbrek hastalığı, aynı zamanda rejeneratif sürecin kaybı ile de tanımlanan bir durumdur (3)(4)(5).…”

Section: Böbrek Dokusundaki Progenitör Benzeri Hücrelerunclassified

Böbrek Kök Hücreleri

Kaya¹,

Şenol²,

Mır³

2017

Turk Neph Dial Transpl

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ÖzBöbrek hastalıkları yüksek morbidite ve mortalite ile ilişkili olan, öncelikli olarak üzerinde çalışılması gereken hastalıklardandır. Akut ve kronik böbrek hastalığının gelişimi renal onarımın işlev gösterememesine bağlıdır. Embriyonik progenitör hücreler nefron epitellerinin çeşitli tiplerine farklanabilen ve çoğalan böbrek hücrelerinin öncüsüdür. Fetal renal progenitör hücreler kısmi olarak kendini yenileme özelliğine sahiptir. İnsanda yetişkin böbrekte tam bir nefron rejenerasyonu mümkün değildir. Progenitör benzeri hücreler sürekli olarak bir hasar ya da fizyolojik bir süreç boyunca kaybolan hücrelerin yerini almaktadır. Bu hücreler in vitro olarak epitelyal ve endotelyal hücrelere dönüştürülmüştür. Kök hücrenin hasarlı böbreğe uygulanması rejeneratif tedavi seçeneklerinden birisidir. Yapılan çalışmalar ile kronik böbrek hastalığının, greft rejeksiyonunun ve diğer böbrek hastalıklarının kök hücre tedavisi ile geri çevrilebileceği, nefron veya diğer yapıların bu tedavi ile yenilenebileceği gösterilmiştir. Böbrek hastalıklarında, organ naklinde ve işlevsel organ üretmede en iyi aday kök hücredir. Bu yöntemin başarısı hücrenin farklanabilme, varolan dokuya girebilme yeteneğine ve renoprotektif faktörleri salgılayabilme kapasitesine bağlıdır. AnAhtAr sözcükler: Kök hücreler, Renal progenitör hücreler, Böbrek rejenerasyonu AbstrActKidney diseases, related to high morbidity and mortality, are one of the diseases that should be primarily investigated. Development of acute and chronic kidney diseases is due to lack of functioning renal repair mechanisms. Embryonic progenitor cells are precursors of renal cells that are able to differentiate to several types of nephron epithelium. Fetal renal progenitor cells are partially capable of self-renewal. In the adult human kidney, whole nephron regeneration is not possible. Progenitor-like cells continuously replace the cells that are lost physiologically or by damage. These cells have been differentiated to epithelial and endothelial cells in vitro. Transplantation of stem cells to the damaged kidney is one of the regenerative therapy options. In recent studies, it has been shown that chronic kidney disease, graft rejection and other kidney diseases could be treated and nephrons and other structures could be regenerated by stem cell therapy. Stem cells are the best candidates for the treatment of kidney diseases, organ transplantation and producing a functional organ. The success of this method is due to the ability of the cells to differentiate, to penetrate the existing tissue and the capacity of the cells to secrete renoprotective factors.

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“…Because of which, substantial efforts are being made to stimulate regeneration with the help of implanted stem cells [3-6]. To provide an effective source and an optimal course of regeneration, different kinds of stem cells were tested and various implantation techniques tried [7, 8]. Although some approaches looked promising, survival of implanted stem cells in the inflammatory environment of a diseased kidney is still unexpectedly limited to a few days [9].…”

mentioning

confidence: 99%

Reading First Coordinates from the Nephrogenic Zone in Human Fetal Kidney

Minuth¹

2017

Nephron

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While substantial information is available on organ anlage and the primary formation of nephrons, molecular mechanisms acting during the late development of the human kidney have received an astonishing lack of attention. In healthy newborn babies, nephrogenesis takes place unnoticed until birth. Upon delivery, morphogenetic activity in the nephrogenic zone decreases, and the stem cell niches aligned beyond the organ capsule vanish by an unknown signal. However, this signal also plays a key role in preterm and low birth weight babies. Although they are born in a phase of active nephrogenesis, pathological findings illustrate that they evolve to a high incidence oligonephropathy and prematurity of renal parenchyma. Different extra- and intrauterine influences seem to be responsible, but independent from chemical nature, all of them culminate in the nephrogenic zone. One assumes that the marred development is caused either by an overshoot of metabolites, misleading signaling of morphogens, unbalanced synthesis of extracellular matrix or restricted contact between mesenchymal and epithelial stem cells. Even more surprising is that there is only a few vague morphological information of the nephrogenic zone in the human fetal kidney available and ultrastructural data is severely lacking. On this account, the first coordinates were determined by optical microscopy and morphometry. Without claiming to be complete, generated results made it possible to create schematic illustrations true to scale for orientation. It will help graduating students, young pediatricians, pathologists, and scientists working in the field of biomedicine to interpret professionally the nephrogenic zone and contained niches.

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Therapeutic use of human renal progenitor cells for kidney regeneration

Abstract: 1415

Cited by 54 publications

References 100 publications

Human CD133+ Renal Progenitor Cells Induce Erythropoietin Production and Limit Fibrosis After Acute Tubular Injury

Human CD133+ Renal Progenitor Cells Induce Erythropoietin Production and Limit Fibrosis After Acute Tubular Injury

Böbrek Kök Hücreleri

Reading First Coordinates from the Nephrogenic Zone in Human Fetal Kidney

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