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","1310"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Periodontology"],["dc.bibliographiccitation.lastpage","1317"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Ziebolz, Dirk"],["dc.contributor.author","Rupprecht, Annegret"],["dc.contributor.author","Schmickler, Jan"],["dc.contributor.author","Bothmann, Laura"],["dc.contributor.author","Krämer, Juliane"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Mausberg, Rainer F."],["dc.contributor.author","Schmidt, Jana"],["dc.contributor.author","Patschan, Susann"],["dc.contributor.author","Schmalz, Gerhard"],["dc.date.accessioned","2021-06-01T10:51:05Z"],["dc.date.available","2021-06-01T10:51:05Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/JPER.17-0616"],["dc.identifier.issn","0022-3492"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86888"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0022-3492"],["dc.title","Association of different immunosuppressive medications with periodontal condition in patients with rheumatoid arthritis: Results from a cross-sectional study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","1201"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.lastpage","1202"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Patschan, Susann"],["dc.contributor.author","Seitz, Cornelia S."],["dc.date.accessioned","2020-12-10T18:27:15Z"],["dc.date.available","2020-12-10T18:27:15Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1111/ddg.13162"],["dc.identifier.issn","1610-0379"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76287"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Haut und Rheuma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.artnumber","952699"],["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Lemmer, D.; 1Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Schmidt, J.; 3Department of Neurology and Pain Treatment, Immanuel Klinik Rüdersdorf, University Hospital of the Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany"],["dc.contributor.affiliation","Kummer, K.; 5Department of Neurology, Neuromuscular Center, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Lemmer, B.; 6Department of Physics, Georg-August-University Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Wrede, A.; 7Department of Neuropathology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Seitz, C.; 8Department of Dermatology, Allergology and Venereology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Balcarek, P.; 9Department of Trauma Surgery, Orthopedics and Plastic Surgery, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Schwarze, K.; 1Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Müller, G. A.; 1Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Patschan, D.; 4Faculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany"],["dc.contributor.affiliation","Patschan, S.; 4Faculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany"],["dc.contributor.author","Lemmer, D."],["dc.contributor.author","Schmidt, J."],["dc.contributor.author","Kummer, K."],["dc.contributor.author","Lemmer, B."],["dc.contributor.author","Wrede, A."],["dc.contributor.author","Seitz, C."],["dc.contributor.author","Balcarek, P."],["dc.contributor.author","Schwarze, K."],["dc.contributor.author","Müller, G. A."],["dc.contributor.author","Patschan, D."],["dc.contributor.author","Patschan, S."],["dc.date.accessioned","2022-12-01T08:31:33Z"],["dc.date.available","2022-12-01T08:31:33Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:29Z"],["dc.description.abstract","Background and aim\r\n Inflammatory myopathies are heterogeneous in terms of etiology, (immuno)pathology, and clinical findings. Endothelial cell injury, as it occurs in DM, is a common feature of numerous inflammatory and non-inflammatory vascular diseases. Vascular regeneration is mediated by both local and blood-derived mechanisms, such as the mobilization and activation of so-called proangiogenic cells (PACs) or early endothelial progenitor cells (eEPCs). The current study aimed to evaluate parameters of eEPC integrity in dermatomyositis (DM), compared to necrotizing myopathy (NM) and to non-myopathic controls.\r\n \r\n \r\n Methods\r\n \r\n Blood samples from DM and NM patients were compared to non-myositis controls and analyzed for the following parameters: circulating CD133\r\n +\r\n /VEGFR-2\r\n +\r\n cells, number of colony-forming unit endothelial cells (CFU-ECs), concentrations of angiopoietin 1, vascular endothelial growth factor (VEGF), and CXCL-16. Muscle biopsies from DM and NM subjects underwent immunofluorescence analysis for CXCR6, nestin, and CD31 (PECAM-1). Finally, myotubes, derived from healthy donors, were stimulated with serum samples from DM and NM patients, subsequently followed by RT-PCR for the following candidates: IL-1β, IL-6, nestin, and CD31.\r\n \r\n \r\n \r\n Results\r\n \r\n Seventeen (17) DM patients, 7 NM patients, and 40 non-myositis controls were included. CD133\r\n +\r\n /VEGFR-2\r\n +\r\n cells did not differ between the groups. Both DM and NM patients showed lower CFU-ECs than controls. In DM, intramuscular CD31 abundances were significantly reduced, which indicated vascular rarefaction. Muscular CXCR6 was elevated in both diseases. Circulating CXCL-16 was higher in DM and NM in contrast, compared to controls. Serum from patients with DM but not NM induced a profound upregulation of mRNS expression of CD31 and IL-6 in cultured myotubes.\r\n \r\n \r\n \r\n Conclusion\r\n Our study demonstrates the loss of intramuscular microvessels in DM, accompanied by endothelial activation in DM and NM. Vascular regeneration was impaired in DM and NM. The findings suggest a role for inflammation-associated vascular damage in the pathogenesis of DM."],["dc.identifier.doi","10.3389/fneur.2022.952699"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118201"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1664-2295"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Impairment of muscular endothelial cell regeneration in dermatomyositis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","45"],["dc.bibliographiccitation.journal","Arthritis Research & Therapy"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Blaschke, Sabine"],["dc.contributor.author","Rinke, Kathinka"],["dc.contributor.author","Maring, Michael"],["dc.contributor.author","Flad, Thomas"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Mueller, Claudia A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Dihazi, Hassan"],["dc.date.accessioned","2018-11-07T09:59:46Z"],["dc.date.available","2018-11-07T09:59:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Introduction: The introduction of tumor necrosis factor-alpha (TNF-alpha) antagonists has substantially improved patient's clinical outcome in rheumatoid arthritis (RA). However, nearly 20% to 40% of RA patients do not respond to anti-TNF-alpha treatment strategies. To identify valid predictors of TNF-alpha antagonist response in RA, serum proteome profiles from responders (R) and non-responders (NR) to etanercept, a soluble recombinant TNF-alpha receptor/IgG Fc fusion protein receptor, were compared in a prospective cohort study. Methods: In this clinical study 50 RA patients with inadequate response to conventional DMARDs were included and treated with etanercept. The primary efficacy endpoint was response according to the European League against Rheumatism (EULAR) improvement criteria. Serum samples collected prior to initiation and after six months of etanercept therapy were cleared of the most abundant major proteins by immunoaffinity chromatography. After separation by two-dimensional differential gel electrophoresis (2D-DIGE) and identification by mass spectrometry (MS) data were validated by Western blot analysis. Results: After six months of etanercept treatment 62% (n = 31) of RA patients achieved response. Haptoglobin-alpha 1 (Hp-alpha 1) and -alpha 2 (Hp-alpha 2) and vitamin D-binding protein (VDBP) were found to be significantly upregulated in responder sera (P <= 0.02) at study entry. In contrast, apolipoprotein C-III (ApoC-III) showed significantly higher levels in non-responders (P = 0.0162). At study end ApoA-II, Hp-alpha 1, Hp-alpha 2 and VDBP were identified to be expressed at significantly higher levels (P < 0.05) in responder sera. Conclusions: By application of clinical proteomics in immunodepleted sera we could identify and validate for the first time Hp-alpha 1, -alpha 2, VDBP and ApoC-III as potential biomarkers for prediction of etanercept drug response in RA."],["dc.description.sponsorship","Pfizer Research Initiative"],["dc.identifier.doi","10.1186/s13075-015-0553-1"],["dc.identifier.isi","000352187400001"],["dc.identifier.pmid","25884688"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13467"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37661"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1478-6362"],["dc.relation.issn","1478-6354"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Haptoglobin-alpha 1, -alpha 2, vitamin D-binding protein and apolipoprotein C-III as predictors of etanercept drug response in rheumatoid arthritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]