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","667"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.bibliographiccitation.lastpage","674"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Backhaus, Rico"],["dc.contributor.author","Elle, Hans-Joerg"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Becker, Jan Ulrich"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.date.accessioned","2018-11-07T09:22:41Z"],["dc.date.available","2018-11-07T09:22:41Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Early endothelial outgrowth cells (eEOCs) significantly protect mice from acute kidney injury (AKI). Angiopoietin-2 (Ang-2) has been shown to be critically involved in vascular repair and homeostasis. The aim of this study was to investigate consequences of Ang-2 treatment of syngeneic murine eEOCs in a cell-based therapeutic approach for AKI. Methods: Male 8- to 12-week-old C57/Bl6N mice, subjected to unilateral renal ischemia (40 minutes) postuninephrectomy were systemically injected with 0.5 x 10(6) untreated or Ang-2-pretreated syngeneic murine eEOCs. Renal function and morphology were analyzed 48 hours later. Cellular consequences of eEOC treatment with Ang-2 were evaluated using different in vitro assays (direct and indirect migration, apoptosis/necrosis, ELISA studies). Results: Administration of untreated eEOCs did not protect mice from AKI. Ang-2 dose-dependently modulated cell effects in AKI. While incubating the cells at a concentration of 200 ng/mL (1 hour) did not have any effect on renal function, doubling the concentration (400 ng/mL) resulted in significant renoprotection of cell-injected mice. With 800 ng/mL, cell injection dramatically worsened renal function of treated animals. In vitro analysis showed significantly accelerated migration of cultured mature endothelial cells after incubation with supernatant from Ang-2-treated eEOCs (200 and 400 ng/mL). These effects were most pronounced with 400 mg/mL. In addition, Ang-2 promoted survival of eEOCs. Cellular releases of VEGF and IL-6 were decreased by Ang-2, while TGF-beta levels in the medium of Ang-2-stimulated eEOCs were not different from those in untreated cells. Conclusion: Ang-2 acts as modulator of eEOCs in AKI. The migration analysis indicates that the Ang-2 significantly alters indirect (paracrine) activity of eEOCs, thus promoting renoprotection in a dose-dependent manner."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.5301/jn.5000255"],["dc.identifier.isi","000325199500012"],["dc.identifier.pmid","23475469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29407"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wichtig Editore"],["dc.relation.issn","1121-8428"],["dc.title","Angiopoietin-2 modulates eEOC-mediated renoprotection in AKI in a dose-dependent manner"],["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","1065"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.bibliographiccitation.lastpage","1072"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Potulski, Marta"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Scholze, Juergen"],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.date.accessioned","2018-11-07T09:17:43Z"],["dc.date.available","2018-11-07T09:17:43Z"],["dc.date.issued","2013"],["dc.description.abstract","Background and aim: Systemic lupus erythematosus (SLE) is an autoimmune-mediated disease, characterized by inflammation of small arteries and arterioles. Patients with SLE suffer from a 17-fold higher risk for developing atherosclerosis than healthy individuals. Endothelial progenitor cells (EPCs) have been shown to be critically involved in microvascular repair under both physiological and pathological conditions. The aim of the present study was to analyze EPC regeneration and mobilization in SLE patients with variable disease activity and undergoing different treatment regimens. Methods: Forty-eight patients with SLE were analyzed. Healthy, age- and sex-matched individuals served as controls. Total circulating EPCs were enumerated by FACS analysis, and regenerative activity of the cells was analyzed by a colony-forming assay. Vasomodulatory mediators were quantified by ELISA. Results: SLE patients did not show lower or higher percentages of total circulating EPCs, but they displayed significantly lower colony numbers as compared with healthy controls, indicating impaired EPC regeneration and mobilization. Low and high disease activity were associated with decreased EPC regeneration, while moderate disease activity was not. Hypertension and, to some extent, renal involvement were associated with reduced colony formation. Patients not receiving hydroxychloroquine (HCQ) treatment and those undergoing glucocorticoid therapy showed impaired EPC regeneration as well. Conclusions: SLE patients suffer from both defective regeneration and mobilization of EPCs. Such an impairment of the EPC system, as one key regulatory element in the process of vasorepair, could potentially promote microvascular damage in SLE. Long-term glucocorticoid therapy may further suppress the EPC system, while HCQ may prevent regeneration of the cells."],["dc.description.sponsorship","Heidenreich von Siebold Program"],["dc.identifier.doi","10.5301/jn.5000273"],["dc.identifier.isi","000331853800013"],["dc.identifier.pmid","24052468"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28232"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wichtig Editore"],["dc.relation.issn","1724-6059"],["dc.relation.issn","1121-8428"],["dc.title","Endothelial progenitor cells in systemic lupus erythematosus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","149"],["dc.bibliographiccitation.journal","Zeitschrift für Rheumatologie"],["dc.bibliographiccitation.lastpage","150"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Mueller, G."],["dc.date.accessioned","2018-11-07T09:20:03Z"],["dc.date.available","2018-11-07T09:20:03Z"],["dc.date.issued","2013"],["dc.identifier.isi","000331709100304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28788"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1435-1250"],["dc.relation.issn","0340-1855"],["dc.title","Patients with limited and systemic Course of systemic Sclerosis (SS) present a perturbed Regeneration of Endothelial Progenitor Cell System"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["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, G."],["dc.date.accessioned","2018-11-07T10:15:53Z"],["dc.date.available","2018-11-07T10:15:53Z"],["dc.date.issued","2016"],["dc.format.extent","S18"],["dc.identifier.isi","000375417500030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40910"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Endothelial-to-Mesenchymal Transition and endothelial cilia in EPC-mediated postischemic kidney protection"],["dc.type","conference_abstract"],["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","S15"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","S16"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Vogt, M."],["dc.contributor.author","Bakhtiari, D."],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Mueller, G."],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T10:15:53Z"],["dc.date.available","2018-11-07T10:15:53Z"],["dc.date.issued","2016"],["dc.identifier.isi","000375417500024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40911"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Endothelial Progenitor Cells in axial Spondyloarthritis"],["dc.type","conference_abstract"],["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"]]