Patschan, Susann Andrea

[["dc.bibliographiccitation.firstpage","F686"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","F694"],["dc.bibliographiccitation.volume","307"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Becker, J. U."],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:35:14Z"],["dc.date.available","2018-11-07T09:35:14Z"],["dc.date.issued","2014"],["dc.description.abstract","Diabetic nephropathy is the most frequent single cause of end-stage renal disease in our society. Microvascular damage is a key event in diabetes-associated organ malfunction. Early endothelial outgrowth cells (eEOCs) act protective in murine acute kidney injury. The aim of the present study was to analyze consequences of eEOC treatment of murine diabetic nephropathy with special attention on endothelial-to-mesenchymal transdifferentiation, autophagy, senescence, and apoptosis. Male C57/Bl6N mice (8-12 wk old) were treated with streptozotocin for 5 consecutive days. Animals were injected with untreated or bone morphogenetic protein (BMP)-5-pretreated syngeneic murine eEOCs on days 2 and 5 after the last streptozotocin administration. Four, eight, and twelve weeks later, animals were analyzed for renal function, proteinuria, interstitial fibrosis, endothelial-to-mesenchymal transition, endothelial autophagy, and senescence. In addition, cultured mature murine endothelial cells were investigated for autophagy, senescence, and apoptosis in the presence of glycated collagen. Diabetes-associated renal dysfunction (4 and 8 wk) and proteinuria (8 wk) were partly preserved by systemic cell treatment. At 8 wk, antiproteinuric effects were even more pronounced after the injection of BMP-5-pretreated cells. The latter also decreased mesenchymal transdifferentiation of the endothelium. At 8 wk, intrarenal endothelial autophagy (BMP-5-treated cells) and senescence (native and BMP-5-treated cells) were reduced. Autophagy and senescence in/of cultured mature endothelial cells were dramatically reduced by eEOC supernatant (native and BMP-5). Endothelial apoptosis decreased after incubation with eEOC medium (native and BMP-5). eEOCs act protective in diabetic nephropathy, and such effects are significantly stimulated by BMP-5. The cells modulate endothelial senescence, autophagy, and apoptosis in a protective manner. Thus, the renal endothelium could serve as a therapeutic target in diabetes-associated kidney dysfunction."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.1152/ajprenal.00650.2013"],["dc.identifier.isi","000341704300008"],["dc.identifier.pmid","25080521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32341"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1522-1466"],["dc.relation.issn","1931-857X"],["dc.title","eEOC-mediated modulation of endothelial autophagy, senescence, and EnMT in murine diabetic nephropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","180"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Apheresis"],["dc.bibliographiccitation.lastpage","185"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T08:34:48Z"],["dc.date.available","2018-11-07T08:34:48Z"],["dc.date.issued","2009"],["dc.description.abstract","Background and Aim: Endothelial progenitor cells (EPCs) have been shown to promote neovascularization under physiologic and pathologic conditions. Statins have been documented to increase the total number of circulating EPCs in long-term treated patients. Lipid apheresis is used to treat patient with refractory hyperlipidemia. The aim of our study was to evaluate whether lipid apheresis is associated with EPC mobilization. Methods: Thirteen patients with refractory hyperlipidemia (analysis at the beginning and at the end of a single lipid apheresis treatment) and 10 healthy controls were included into the study. For quantifying total peripheral EPCs, CD133+/Flk-1+ myelo-monocytic blood cells were enumerated by flow cytometry. The proliferative potential of EPCs was evaluated by a \"colony-forming unit\" assay. In some patients, EPC eNOS expression was evaluated before and after treatment. Results: Circulating EPCs and the cells' proliferative activity were lower in hyperlipidemia patients as compared to controls (0.14 +/- 0.07 vs. 0.6 +/- 0.14, P = 0.01, and 13.9 +/- 4.9 vs. 45.6 +/- + 8.1. P = 0.0007). Lipid apheresis treatment was not associated with an increase in total EPCs. The cells' proliferative activity was strongly stimulated by lipid apheresis as reflected by an increase in the number of EPC colonies (13.9 +/- 4.9 to 34.1 +/- 7.1 P = 0.035). Analysis of EPC eNOS expression revealed a threefold increase in the cellular expression intensity after lipid apheresis. Conclusions: Patients with refractory hyperlipidemia exhibit lower peripheral EPC numbers and a lower proliferative activity of circulating EPCs than healthy controls. A single lipid apheresis treatment significantly stimulates EPC proliferation. it furthermore increases cellular eNOS. In summary, these results show that lipid apheresis mediates beneficial effects on the EPC system as an essential element in the process of vascular repair in the human organism. J. Clin. Apheresis 24:180-185. 2009. (C) 2009 Wiley-Liss, Inc."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [PA1530/2-1, PA1530/3-1]"],["dc.identifier.doi","10.1002/jca.20208"],["dc.identifier.isi","000271446400002"],["dc.identifier.pmid","19753649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17907"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0733-2459"],["dc.title","LDL Lipid Apheresis Rapidly Increases Peripheral Endothelial Progenitor Cell Competence"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","F679"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","F687"],["dc.bibliographiccitation.volume","310"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T10:16:23Z"],["dc.date.available","2018-11-07T10:16:23Z"],["dc.date.issued","2016"],["dc.description.abstract","Renal ischemia induces peritubular capillary rarefication and fibrosis, with the latter partly resulting from the endothelial-to-mesenchymal transition (EndoMT). Endothelial cilia transmit blood flow-associated forces into the cell. Early endothelial progenitor cells (eEPCs) have been shown to protect mice from acute kidney injury in the short term. The aim of the present study was to analyze midterm consequences of eEPC treatment in the context of endothelial cilia and the EndoMT. Male C57/Bl6N mice were subjected to unilateral renal ischemia postuninephrectomy. Syngeneic murine eEPCs were systemically injected at the time of reperfusion. Animals were investigated 1, 4, and 6 wk later. Cultured mature endothelial cells were exposed to a variable flow with versus without eEPC supernatant incubation. Systemically injected eEPCs reduced serum creatinine levels at week 1 (35 and 45 min) and week 4 (45 min). Interstitial fibrosis was significantly diminished by cell treatment at all time points as well. The EndoMT was less pronounced at week 4 (35 min) and week 6 (45 min). eEPC supernatant reduced alpha-smooth muscle actin expression and alpha-tubulin abundance in flow-treated cultured mature endothelial cells, and percentages of cilium-positive cells increased. The loss of peritubular capillaries was prevented by eEPCs. Intrarenal endothelial alpha-tubulin decreased postischemia and was further reduced by eEPC administration. We conclude that eEPCs are capable of reorganizing the endothelial cytoskeleton in an indirect manner, ultimately resulting in stabilization of the endothelial ciliome. The investigation indicates an antimesenchymal role of endothelial cilia in the process of postischemic tissue fibrosis/EndoMT."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; Jackstadt-Stiftung"],["dc.identifier.doi","10.1152/ajprenal.00306.2015"],["dc.identifier.isi","000373269900010"],["dc.identifier.pmid","26792062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41027"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1522-1466"],["dc.relation.issn","1931-857X"],["dc.title","The endothelial-to-mesenchymal transition and endothelial cilia in EPC-mediated postischemic kidney protection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","F314"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","F322"],["dc.bibliographiccitation.volume","305"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Lange, Andrea"],["dc.contributor.author","Meise, Nyree"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Becker, Jan Ulrich"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:21:49Z"],["dc.date.available","2018-11-07T09:21:49Z"],["dc.date.issued","2013"],["dc.description.abstract","Early endothelial outgrowth cells (eEOCs) reproducibly have been shown to act protectively in acute ischemic kidney injury (AKI) and chronic kidney injury. Bone morphogenetic protein-5 (BMP-5) acted antifibrotically in human hypertensive nephropathy. The aim of the curent study was to analyze effects of BMP-5 treatment in an eEOC-based therapy of murine AKI and 5/6-nephrectomy. Male C57/Bl6N mice were either subjected to unilateral renal artery clamping postuninephrectomy or to 5/6-nephrectomy. Untreated or BMP-5-pretreated murine eEOCs were injected into recipient animals at the time of reperfusion (AKI) or at 2 and 5 days after 5/6-nephrectomy. Analysis of renal function and morphology was performed at 48 h and at 6 wk (AKI) or at 8 wk (5/6 model). Cellular consequences of eEOC treatment were evaluated using different in vitro assays. AKI was mitigated significantly by injecting BMP-5-pretreated eEOCs. Renal function was improved at 48 h and at 6 wk after cell therapy. In 5/6-nephrectomy, the cells failed to protect renal function, but proteinuria was reduced after administering untreated eEOCs. BMP-5 pretreatment resulted in aggravated proteinuria and renal fibrosis. In 5/6-nephrectomized animals, percentages of anti-smooth muscle actin +/CD31+ cells increased, indicating endothelial-mesenchymal transition (EnMT). In vitro analysis revealed increased cell migration and reduced cell apoptosis/necrosis. Paracrinic activity remained unaffected. BMP-5 acts as a potent eEOC agonist in murine AKI in the short and mid to long term. Cell effects in 5/6-nephrectomy are heterogenous, but untreated cells act antiproteinurically and antifibrotically without any impact on EnMT."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.1152/ajprenal.00677.2012"],["dc.identifier.isi","000322699000011"],["dc.identifier.pmid","23678046"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29196"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1931-857X"],["dc.title","Bone morphogenetic protein-5 and early endothelial outgrowth cells (eEOCs) in acute ischemic kidney injury (AKI) and 5/6-chronic kidney disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","528"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Scandinavian Journal of Rheumatology"],["dc.bibliographiccitation.lastpage","530"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Nemirovsky, K."],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Scholze, Juergen"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T09:45:37Z"],["dc.date.available","2018-11-07T09:45:37Z"],["dc.date.issued","2014"],["dc.identifier.isi","000345854600015"],["dc.identifier.pmid","25222920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34666"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1502-7732"],["dc.relation.issn","0300-9742"],["dc.title","Tocilizumab increases EPC regeneration in rheumatoid arthritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","F78"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","F85"],["dc.bibliographiccitation.volume","298"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Becker, J. U."],["dc.contributor.author","David, S."],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Goligorsky, Michael S."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T08:46:55Z"],["dc.date.available","2018-11-07T08:46:55Z"],["dc.date.issued","2010"],["dc.description.abstract","Patschan D, Patschan S, Wessels JT, Becker JU, David S, Henze E, Goligorsky MS, Muller GA. Epac-1 activator 8-O-cAMP augments renoprotective effects of allogeneic murine EPCs in acute ischemic kidney injury. Am J Physiol Renal Physiol 298: F78-F85, 2010. First published November 11, 2009; doi:10.1152/ajprenal.00485.2009.-Endothelial progenitor cells (EPCs) protect kidneys from acute ischemic damage. The aim of this study was to identify \"treatment parameters\" that optimize an EPC-based therapy of acute ischemic renal failure. Male C57BL/6N mice underwent unilateral nephrectomy with simultaneous contralateral renal artery clamping for 30, 35, and 40 min. Tagged murine EPCs were systemically injected at the time of reperfusion. In some experiments, EPCs were pretreated with the Epac (exchange protein directly activated by cAMP-1) activator 8-pCPT-2'-O-Me-cAMP (Epac-1 Ac) and the integrin binding antagonist cyclic Arg-Gly-Asp peptide (cRGD). Injections of 106 EPCs after 30 and 35 min of renal ischemia protected animals from acute renal failure. The same effect occurred with 0.5x10(6) EPCs after a 35-min period of ischemia. If ischemia lasted for 40 min, 0.5x10(6) cells mice did not prevent acute renal failure. To analyze whether EPC integrin receptor activation would modify the cells' renoprotective activity, EPCs were pretreated with Epac-1 Ac. Such animals did not develop acute renal failure, even if ischemia lasted for 40 min. This effect was negated if the cells were pretreated with both Epac-1 Ac and cRGD. In kidneys from those animals medullopapillary EPCs were significantly accumulated. In vitro Epac-1 Ac preactivation of EPCs did not increase the overall expression intensity but induced a redistribution of beta(1)-integrins toward the cell membranes. We conclude that EPC pretreatment with the integrin receptor activator 8-pCPT-2'-O-Me-cAMP augments the anti-ischemic potential of the cells."],["dc.identifier.doi","10.1152/ajprenal.00485.2009"],["dc.identifier.isi","000272924500010"],["dc.identifier.pmid","19906949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20811"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1931-857X"],["dc.title","Epac-1 activator 8-O-cAMP augments renoprotective effects of allogeneic murine EPCs in acute ischemic kidney injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","368"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Periodontology"],["dc.bibliographiccitation.lastpage","379"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Schmickler, Jan"],["dc.contributor.author","Rupprecht, Annegret"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Haak, Rainer"],["dc.contributor.author","Mausberg, Rainer F."],["dc.contributor.author","Schmalz, Gerhard"],["dc.contributor.author","Kottmann, Tanja"],["dc.contributor.author","Ziebolz, Dirk"],["dc.date.accessioned","2018-11-07T10:25:46Z"],["dc.date.available","2018-11-07T10:25:46Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: This study evaluates periodontal conditions and microbiologic findings and their influence on rheumatologic disease parameters in patients with rheumatoid arthritis (RA). Methods: One hundred and sixty-eight patients with RA were included. A healthy control group (HC, n = 168) was composed according to age, sex, and smoking habits. Rheumatologic data (duration of illness, Disease Activity Score 28, rheumatic factor [RF], anti-cyclic citrullinated peptide [aCCP], medications) were extracted from patients' records. Dental examination included: 1) dental findings (decayed, missing, and/or filled adult teeth [DMF-T] index); 2) gingival inflammation (papillary bleeding index [PBI]); and 3) periodontal status (probing depth [PD], attachment loss [AL]). Periodontal condition was classified as healthy/mild, moderate, or severe periodontitis. Subgingival biofilm was analyzed regarding 11 periodontopathogenic bacteria. Statistical analyses included: 1) Kolmogorov-Smirnov test; 2) MannWhitney U test; 3) Pearson x(2) test; 4) Kruskal-Wallis test; and 5) regression analysis; level of significance alpha = 5%. Results: Mean DMF-T was significantly higher in patients with RA (19.3 +/- 4.8) than in HC group (16.9 +/- 5.8), especially owing to number of missing teeth (RA = 6.0 +/- 5.4, HC = 3.1 +/- 3.3; P < 0.01). Patients with RA had a significantly higher proportion of increased PD (P < 0.01) and AL compared with HC group (P < 0.01). Moderate to severe periodontitis was noted in 98% of patients with RA and 82% of the HC group (P < 0.01). RF-positive patients with RA suffered from worse periodontal conditions than RF-negative patients (P = 0.01). Age, PBI, and presence of Treponema denticola (P < 0.03) are related to periodontal condition in patients with RA. Although not statistically significant, Porphyromonas gingivalis and Fusobacterium nucleatum occur in higher concentrations more often in aCCP-positive patients with RA (P = 0.06). Conclusions: Patients with RA had worse periodontal conditions than HC participants. Although a trend for higher F. nucleatum and P. gingivalis concentrations in aCCP-positive patients with RA was found, importance of periodontal pathogenic bacteria and rheumatoid parameters in the interrelationship between periodontitis and RA remains unclear."],["dc.identifier.doi","10.1902/jop.2016.160355"],["dc.identifier.isi","000398260300009"],["dc.identifier.pmid","27858553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42921"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Acad Periodontology"],["dc.relation.issn","1943-3670"],["dc.relation.issn","0022-3492"],["dc.title","Cross-Sectional Evaluation of Periodontal Status and Microbiologic and Rheumatoid Parameters in a Large Cohort of Patients With Rheumatoid Arthritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","F1305"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","F1312"],["dc.bibliographiccitation.volume","302"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Hildebrandt, A."],["dc.contributor.author","Rinneburger, Joerg"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Becker, J. U."],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Krueger, A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:10:41Z"],["dc.date.available","2018-11-07T09:10:41Z"],["dc.date.issued","2012"],["dc.description.abstract","Patschan D, Hildebrandt A, Rinneburger J, Wessels JT, Patschan S, Becker JU, Henze E, Kruger A, Muller GA. The hormone melatonin stimulates renoprotective effects of \"early outgrowth\" endothelial progenitor cells in acute ischemic kidney injury. Am J Physiol Renal Physiol 302: F1305-F1312, 2012. First published February 22, 2012; doi:10.1152/ajprenal.00445.2011.-Endothelial progenitor cells (EPCs) protect the kidney from acute ischemic injury. The aim of this study was to analyze whether pretreatment of murine \"early outgrowth\" EPCs (eEPCs) with the hormone melatonin increases the cells' renoprotective effects in the setting of murine acute ischemic renal failure. Male (8-12 wk old) C57B1/6N mice were subjected to unilateral ischemia-reperfusion injury postuninephrectomy (40 min). Postischemic animals were injected with either 0.5 x 10(6) untreated syngeneic murine eEPCs or with cells, pretreated with melatonin for 1 h. Injections were performed shortly after reperfusion of the kidney. While animals injected with untreated cells developed acute renal failure, eEPC pretreatment with melatonin dramatically improved renoprotective actions of the cells. These effects were completely reversed after cell pretreatment with melatonin and the MT-1/-2 antagonist luzindole. In vitro analysis revealed that melatonin reduced the amount of tumor growth factor-beta-induced eEPC apoptosis/necrosis. Secretion of vascular endothelial growth factor by the cells was markedly stimulated by the hormone. In addition, migratory activity of eEPCs was enhanced by melatonin and supernatant from melatonin-treated eEPCs stimulated migration of cultured mature endothelial cells. In summary, melatonin was identified as a new agonist of eEPCs in acute ischemic kidney injury."],["dc.identifier.doi","10.1152/ajprenal.00445.2011"],["dc.identifier.isi","000304356400011"],["dc.identifier.pmid","22357919"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26548"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1931-857X"],["dc.title","The hormone melatonin stimulates renoprotective effects of \"early outgrowth\" endothelial progenitor cells in acute ischemic kidney injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]