Angiopoietin-2 modulates eEOC-mediated renoprotection in AKI in a dose-dependent manner

Patschan, Daniel; Backhaus, Rico; Elle, Hans-Jörg; Schwarze, Katrin; Henze, Elvira; Becker, Jan U.; Patschan, Susann; Müller, Gerhard A.

doi:10.5301/jn.5000255

Cited by 23 publications

(29 citation statements)

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“…9,37 In the present study, human umbilical cord blood-derived ECFCs lacked hematopoietic markers (ie, CD45 and CD14) and displayed exclusively markers of endothelial lineage. In NOD-SCID mice, we observed that ECFCs attenuated I/R-induced renal injury, as determined by decreases in plasma creatinine.…”

Section: Protective Effects Of Human Ecfcs In Renal I/r Injurymentioning

confidence: 97%

Human Endothelial Colony-Forming Cells Protect against Acute Kidney Injury

Burger

Viñas

Akbari

et al. 2015

The American Journal of Pathology

196

181

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The administration of certain progenitor cells is protective in experimental acute kidney injury (AKI), and mechanisms may involve the release of paracrine factors. Endothelial colony-forming cells (ECFCs) are endothelial precursor cells with a high proliferative capacity and pro-angiogenic potential. We examined the effects of human umbilical cord blood-derived ECFCs and their extracellular vesicles in a mouse model of ischemic AKI and in cultured human umbilical vein endothelial cells subjected to hypoxia/reoxygenation. In mice with ischemic AKI, administration of ECFCs (i.v.) at the time of reperfusion significantly attenuated increases in plasma creatinine, tubular necrosis, macrophage infiltration, oxidative stress, and apoptosis, without cell persistence in the kidneys. In cultured human umbilical vein endothelial cells, hypoxia/reoxygenation stimulated apoptosis. This effect was inhibited by incubation with conditioned medium or exosomes (40- to 100-nm diameter) derived from ECFCs, but not by microparticles (100- to 1000-nm diameter) or vesicle-depleted conditioned medium. Administration of exosomes (i.v.) directly to mice with ischemic AKI attenuated renal injury, as assessed by plasma creatinine, tubular necrosis, and apoptosis. Taken together, these studies indicate protective effects of human cord blood-derived ECFCs in experimental AKI and suggest that ECFC-derived exosomes may mediate the protective response via inhibition of endothelial cell apoptosis.

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Section: Protective Effects Of Human Ecfcs In Renal I/r Injurymentioning

confidence: 97%

Human Endothelial Colony-Forming Cells Protect against Acute Kidney Injury

Burger

Viñas

Akbari

et al. 2015

The American Journal of Pathology

196

181

View full text Add to dashboard Cite

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“…Thus, further studies were intended to augment the AKI-protective capacity of PACs and several pharmacological agonists of the cells were identified. Among those were melatonin [47], 8-O-cAMP [51], Bone Morphogenetic Protein-5 (BMP-5) [46], and Angiopoietin-1 [50] and -2 [49]. A more recent study showed that PACs administration post-AKI did not only prevent the kidney from acute loss of excretory function but also stabilizeed certain structural outcome parameters such as interstitial fibrosis and loss of peritubular capillaries [52].…”

Section: Proangiogenic Cells (Pacs) and Endothelial Colony Forming Cementioning

confidence: 99%

“…Both subpopulations, PACs and ECFCs have sucessfully been administered in experimental AKI [44-48]. In addition, several strategies have been established in order to augment AKI-protective effects of particularly PACs [46, 47, 49-51]. In almost all of the mentioned studies, kidney excretory function was evaluated by serum creatinine levels and additionally by certain morphological parameters such as acute tubular damage shortly (48 hours) after ischemia.…”

Section: Proangiogenic Cells (Pacs) and Endothelial Colony Forming Cementioning

confidence: 99%

Cell-Based Therapies in Acute Kidney Injury (AKI)

Patschan

Buschmann

Ritter

et al. 2018

Kidney Blood Press Res

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Acute kidney injury frequently occurs in hospitalized patients all over the world. The prognosis remains poor since specific therapies for promoting kidney regeneration/repair are still missing. In recent years cell-based strategies have improved AKI outcomes under experimental circumstances. Four groups of cells, each of them displaying certain biological and functional characteristics have been evaluated in AKI, induced Pluripotent Stem Cells (iPSCs), Spermatagonial Stem Cells (SSCs), Proangiogenic Cells (PACs) and Endothelial Colony Forming Cells (ECFCs), and Mesenchymal Stem Cells (MSCs). All of these have been documented to stabilize either parameters of kidney excretory dysfunction and/or certain morphological parameters. The mechanisms responsible for AKI protection include direct (cell incorporation) and indirect processes, the latter being mediated by humoral factors and particularly by the production of so-called extracellular vesicles. Cell-derived vesicular organelles have been shown to carry pro-regenerative micro-RNA molecules which stabilize the vascular and tubular function. The first trials in humans have been initiated, the majority of such trials employs MSCs. However, any transfer of cell-based strategies in the clinical practice is potentially associated with significant difficulties. These include cell availability, tolerance and competence. The article intends to summarize essential informations about all of the four populations mentioned above and to discuss implications for the management of human AKI.

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“…In vivo, ANG2 enhances the proliferative capacity of EPCs [131]. Furthermore, Patschan et al showed that stimulation of EPCs with ANG2 ex vivo prior to transplantation significantly increased their protective effects on renal I/R injury in mice [145]. Dosage likewise plays a crucial role, as either too low or too high concentrations had no positive, or even a pronounced negative effect.…”

Section: Therapeutic Effects Of Ang2mentioning

confidence: 95%