Patschan, Daniel

[["dc.bibliographiccitation.artnumber","R94"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Johanna, Temme"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:01:04Z"],["dc.date.available","2018-11-07T09:01:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction: Sepsis is characterized by systemic microvascular dysfunction. Endothelial progenitor cells (EPCs) are critically involved in maintaining vascular homeostasis under both physiological and pathological conditions. The aim of the present study was to analyze the endothelial progenitor cell system in patients suffering from sepsis with acute renal dysfunction. Methods: Patients with newly diagnosed sepsis were recruited from the ICU in a nonrandomized prospective manner. Blood samples were obtained within the first 12 hours after the diagnosis of sepsis. For quantifying endothelial progenitor cells (EPCs), CD133(+)/Flk-1(+) cells were enumerated by cytometric analysis. Analysis of EPC proliferation was performed by a colony-forming units (CFU) assay. Blood concentrations of proangiogenic mediators were measured by ELISA. Acute renal dysfunction was diagnosed according to the Acute Kidney Injury Network (AKIN) criteria. Depending on the overall mean creatinine concentration during the stay at the ICU, patients were either assigned to a 'normal creatinine group' or to a 'high creatinine group'. Survival rates, frequency of dialysis, the simplified acute physiology score (SAPS) II scores, and different laboratory parameters were collected/used for further clinical characterization Results: Circulating EPCs were significantly higher in all sepsis patients included in the study as opposed to healthy controls. Patients within the 'high creatinine group' showed an even more pronounced EPC increase. In contrast, EPC proliferation was severely affected in sepsis. Neither total circulating EPCs nor EPC proliferation differed between patients requiring dialysis and patients without renal replacement therapy. Cell numbers and cell proliferation also did not differ between surviving patients and patients with sepsis-related death. Serum levels of vascular endothelial growth factor (VEGF), stromal derived factor-1 (SDF-1), and Angiopoietin-2 were higher in sepsis than in healthy controls. Sepsis patients within the 'high creatinine group' showed significantly higher mean serum levels of uric acid. Conclusions: Sepsis significantly affects the endothelial progenitor cell system, as reflected by increased EPC numbers, increased concentrations of proangiogenic mediators, and reduced proliferative capacity of the cells. This occurs independently from the frequency of dialysis and from patient survival. Increased serum levels of uric acid are possibly responsible for stronger EPC mobilization in sepsis patients with higher average creatinine levels."],["dc.identifier.doi","10.1186/cc10100"],["dc.identifier.isi","000292506000018"],["dc.identifier.pmid","21396100"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24323"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15283 but duplicate"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1466-609X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.holder","Patschan et al.; licensee BioMed Central Ltd."],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Endothelial progenitor cells (EPC) in sepsis with acute renal dysfunction (ARD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","227"],["dc.bibliographiccitation.journal","BMC Nephrology"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Rinneburger, Joerg"],["dc.contributor.author","Idrizi, Nazif"],["dc.contributor.author","Backhaus, Rico"],["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","2018-11-07T09:18:33Z"],["dc.date.available","2018-11-07T09:18:33Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Acute kidney injury (AKI) severely worsens prognosis of hospitalized patients. Early Endothelial Outgrowth Cells act protective in murine acute ischemic renal failure and renoprotective actions of eEOCs have been documented to increase after cell pretreatment with 8-O-cAMP and Melatonin. Angiopoietin-1 is critically involved in maintaining vascular integrity and regeneration. Aim of the study was to analyze the consequences of eEOC treatment with Ang-1 in murine AKI. Methods: After 40 minutes of unilateral renal artery clamping with contralateral nephrectomy, male C57/Bl6N mice were injected with either untreated or pretreated (Ang-1) syngeneic murine eEOCs. Two days later serum creatinine levels and morphology were evaluated. Cultured, Ang-1 treated murine eEOCs were analyzed for production/release of proangiogenic and proinflammatory mediators, migratory activity, and cell survival, respectively. Results: Angiopoietin-1 pretreatment of eEOCs significantly reduced serum creatinine in cell-injected mice. In vitro analysis showed increased migration of Ang-1 treated eEOCs and supernatant from Ang-1 treated eEOCs stimulated migration of cultured mature endothelial cells. In addition, Ang-1 reduced percentages of Annexin V+/PI+ eEOCs. Intrarenal numbers of eEOCs remained unaffected by Ang-1 and eEOCs did not produce more or less proangiogenic/proinflammatory mediators after being stimulated with Ang-1. Conclusions: Angiopoietin-1 pretreatment of eEOCs increases the cells' renoprotective competence in ischemic AKI. Thus, the armentarium of eEOC agonists in AKI is increasingly being expanded and the treatment of AKI with eEOCs becomes a promising future option."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.1186/1471-2369-14-227"],["dc.identifier.isi","000327482300001"],["dc.identifier.pmid","24144241"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28432"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2369"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Angiopoietin-1 treated early endothelial outgrowth cells (eEOCs) are activated in vitro and reduce renal damage in murine acute ischemic kidney injury (iAKI)"],["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"]]

[["dc.bibliographiccitation.firstpage","637"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.bibliographiccitation.lastpage","644"],["dc.bibliographiccitation.volume","29"],["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, Gerhard Anton"],["dc.date.accessioned","2018-11-07T10:08:10Z"],["dc.date.available","2018-11-07T10:08:10Z"],["dc.date.issued","2016"],["dc.description.abstract","Autophagy enables cells to digest endogenous/exogenous waste products, thus potentially prolonging the cellular lifespan. Early endothelial progenitor cells (eEPCs) protect mice from ischemic acute kidney injury (AKI). The mid-term prognosis in AKI critically depends on vascular rarefication and interstitial fibrosis with the latter partly being induced by mesenchymal transdifferentiation of endothelial cells (EndoMT). This study aimed to determine the impact of eEPC preconditioning with different autophagy inducing agents [suberoylanilide hydroxamic acid (SAHA)/temsirolimus] in ischemic AKI. Male C57/Bl6 N mice were subjected to bilateral renal ischemia (40 min). Animals were injected with either untreated, or SAHA- or temsirolimus-pretreated syngeneic murine eEPCs at the time of reperfusion. Mice were analyzed 48 h and 4 weeks later. In addition, cultured eEPCs were treated with transforming growth factor (TGF)-beta +/- SAHA, autophagy (perinuclear LC3-II), and stress-induced premature senescence (SIPS-senescence-associated beta-galactosidase, SA-beta-Gal), and were evaluated 96 h later. Cultured eEPCs showed reduced perinuclear density of LC3-II + vesicles and elevated levels of SA-beta-Gal after treatment with TGF-beta alone, indicating impaired autophagy and aggravated SIPS. These effects were completely abrogated by SAHA. Systemic administration of either SAHA or tems pretreated eEPCs resulted in elevated intrarenal endothelial p62 at 48 h and 4 weeks, indicating stimulated endothelial autophagy. This effect was most pronounced after injection of SAHA-treated eEPCs. At 4 weeks endothelial expression of mesenchymal alpha-smooth muscle actin (alpha SMA) was reduced in animals receiving untreated and SAHA-pretreated cells. In addition, SAHA-treated cells reduced fibrosis at week 4. Tems in contrast aggravated EndoMT. Postischemic renal function declined after renal ischemia and remained unaffected in all experimental cell treatment groups. In ischemic AKI, intrarenal endothelial autophagy may be stabilized by systemic administration of pharmacologically preconditioned eEPCs. Early EPCs can reduce postischemic EndoMT and fibrosis in the mid-term. Autophagy induction in eEPCs either increases or decreases the mesenchymal properties of intrarenal endothelial cells, depending on the substance being used. Thus, endothelial autophagy induction in ischemic AKI, mediated by eEPCs is not a renoprotective event per se."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.1007/s40620-015-0222-0"],["dc.identifier.isi","000383012600006"],["dc.identifier.pmid","26289253"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39417"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wichtig Publishing"],["dc.relation.issn","1724-6059"],["dc.relation.issn","1121-8428"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Endothelial autophagy and Endothelial-to-Mesenchymal Transition (EndoMT) in eEPC treatment of ischemic AKI"],["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"]]

[["dc.bibliographiccitation.artnumber","339"],["dc.bibliographiccitation.journal","BMC Musculoskeletal Disorders"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Mueller, C."],["dc.contributor.author","Seitz, C."],["dc.contributor.author","Herink, Claudia"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T10:10:11Z"],["dc.date.available","2018-11-07T10:10:11Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Patients with systemic sclerosis (SSc) are endagered by tissue fibrosis and by microvasculopathy, with the latter caused by endothelial cell expansion/proliferation. SSc-associated fibrosis potentially results from mesenchymal transdifferentiation of endothelial cells. Early Endothelial Progenitor Cells (eEPCs) act proangiogenic under diverse conditions. Aim of the study was to analyze eEPC regeneration and mesenchymal transdifferentiation in patients with limited and diffuse SSs (lSSc and dSSc). Methods: Patients with both, lSSc and dSSc were included into the study. The following parameters were evaluated: eEPC numbers and regeneration, concentrations of vasomodulatory mediators, mesenchymal properties of blood-derived eEPC. Serum samples of healthy subjects and SS patients were used for stimulation of cultured human eEPC, subsequently followed by analysis of mesenchymal cell characteristics and mobility. Results: Twenty-nine patients were included into the study. Regenerative activity of blood-derived eEPCs did not differ between Controls and patients. Circulating eEPC were significantly lower in all patients with SSc, and in limited and diffuse SSc (lSSc/dSSc). Serum concentrations of promesenchymal TGF-b was elevated in all patients with SSc. Cultured mononuclear cells from SS patients displayed higher abundances of CD31 and of CD31 and aSMA combined. Finally, serum from SSc patients inhibited migration of cultured eEPCs and the cells showed lower sensitivity towards the endothelin antagonist Bosentan. Conclusions: The eEPC system, which represents an essential element of the endogenous vascular repair machinery is affected in SSc. The increased appearance of mesenchymal properties in eEPC may indicate that alterations of the cells potentially contribute to the accumulation of connective tissue and to vascular malfunction."],["dc.description.sponsorship","Heidenreich von-Siebold Programm"],["dc.identifier.doi","10.1186/s12891-016-1197-2"],["dc.identifier.isi","000395017600003"],["dc.identifier.pmid","27519706"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13866"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39808"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2474"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Early Endothelial Progenitor Cells (eEPCs) in systemic sclerosis (SSc) - dynamics of cellular regeneration and mesenchymal transdifferentiation"],["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"]]

[["dc.bibliographiccitation.firstpage","1907"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Rheumatology International"],["dc.bibliographiccitation.lastpage","1917"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Hoffmann, Johanna Charlotte"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Müller, Claudia"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Ritter, Oliver"],["dc.contributor.author","Müller, Gerhard Anton"],["dc.contributor.author","Patschan, Susann"],["dc.date.accessioned","2020-12-10T14:10:11Z"],["dc.date.available","2020-12-10T14:10:11Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00296-019-04364-y"],["dc.identifier.eissn","1437-160X"],["dc.identifier.issn","0172-8172"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70667"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cytokine profiling in anti neutrophil cytoplasmic antibody-associated vasculitis: a cross-sectional cohort study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","International Journal of Nephrology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","2012"],["dc.contributor.author","Patschan, Susann"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Blaschke, Sabine"],["dc.contributor.author","Wessels, Johannes T."],["dc.contributor.author","Müller, Gerhard Anton"],["dc.date.accessioned","2019-07-09T11:53:33Z"],["dc.date.available","2019-07-09T11:53:33Z"],["dc.date.issued","2012"],["dc.description.abstract","Granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) are autoimmune-mediated diseases characterized by vasculitic inflammation of respiratory tract and kidneys. Clinical observations indicated a strong association between disease activity and serumlevels of certain types of autoantibodies (antineutrophil cytoplasm antibodies with cytoplasmic [cANCA in GPA] or perinuclear [pAN CA in MPA] immunofluorescence). Pathologically, both diseases are characterized by severe microvascular endothelial cell damage. Early endothelial outgrowth cells (eEOCs) have been shown to be critically involved in neovascularization under both physiological and pathological condition. Objectives. The principal aims of our study were (i) to analyze the regenerative activity of the eEOC system and (ii) to determine mPR3 and MPO expression in myelo monocytic cells with endothelial characteristics in GPA and MPA patients. Methods. In 27 GPA and 10 MPA patients, regenerative activity bloodderived eEOCs were analyzed using a culture-forming assay. Flk-1+, CD133+/Flk-1+, mPR3+, and Flk-1+/mPR3+ myelomonocytic cells were quantified by FACS analysis. Serum levels of Angiopoietin-1 and TNF-α were measured by ELISA. Results. We found reduced eEOC regeneration, accompanied by lower serum levels of Angiopoietin-1 in GPA patients as compared to healthy controls. In addition, the total numbers of Flk-1+ myelomonocytic cells in the peripheral circulation were decreased. Membrane PR3 expression was significantly higher in total as well as in Flk-1+ myelomonocytic cells. Expression of MPO was not different between the groups. Conclusions. These data suggest impairment of the eEOC system and a possible role for PR3 in this process in patients suffering from GPA."],["dc.identifier.doi","10.1155/2012/715049"],["dc.identifier.fs","592925"],["dc.identifier.pmid","22792461"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60445"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Impairment and Differential Expression of PR3 and MPO on Peripheral Myelomonocytic Cells with Endothelial Properties in Granulomatosis with Polyangiitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e000185"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Lupus Science & Medicine"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Niewold, Timothy B."],["dc.contributor.author","Müller, Gerhard-Anton"],["dc.contributor.author","Patschan, Susann Andrea"],["dc.date.accessioned","2019-07-09T11:45:40Z"],["dc.date.available","2019-07-09T11:45:40Z"],["dc.date.issued","2016"],["dc.description.abstract","Patients with SLE display a significantly higher cardiovascular risk (CVR). Pulse wave velocity (PWV) has meanwhile been established as a reliable parameter of end-organ damage. Endothelial progenitor cells (EPCs) are critically involved in vascular repair under both physiological and pathological conditions. The aim of the study was to analyse PWV and the Vascular Augmentation Index (VAI) and EPC numbers/regeneration in a well-defined German SLE cohort. Thirty patients were included. Only two individuals displayed a PWV of above 10 m/s. There was no correlation between PWV percentiles and disease activity as reflected by the SLE Disease Activity Index. Neither EPC colonies nor percentages of circulating EPCs (CD133+/KDR+) correlated with PWV/VAI in a positive or negative manner. Thus, it can be questioned whether pulse wave analysis and/or EPC proliferation and circulating cell numbers are truly useful for CVR assessment in SLE."],["dc.identifier.doi","10.1136/lupus-2016-000185"],["dc.identifier.pmid","28176918"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15278"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59282"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2053-8790"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Dynamics of pulse wave velocity and vascular augmentation index in association with endothelial progenitor cells in SLE."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]