Frese, Jenny

[["dc.bibliographiccitation.firstpage","131"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Pediatric Nephrology"],["dc.bibliographiccitation.lastpage","137"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Stock, Johanna"],["dc.contributor.author","Kuenanz, Johannes"],["dc.contributor.author","Glonke, Niklas"],["dc.contributor.author","Sonntag, Joseph"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Toenshoff, Burkhard"],["dc.contributor.author","Hoecker, Britta"],["dc.contributor.author","Hoppe, Bernd"],["dc.contributor.author","Feldkoetter, Markus"],["dc.contributor.author","Pape, Lars"],["dc.contributor.author","Lerch, Christian"],["dc.contributor.author","Wygoda, Simone"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2018-11-07T10:29:37Z"],["dc.date.available","2018-11-07T10:29:37Z"],["dc.date.issued","2017"],["dc.description.abstract","Patients with autosomal or X-linked Alport syndrome (AS) with heterozygous mutations in type IV collagen genes have a 1-20 % risk of progressing to end-stage renal disease during their lifetime. We evaluated the long-term renal outcome of patients at risk of progressive disease (chronic kidney disease stages 1-4) with/without nephroprotective therapy. This was a prospective, non-interventional, observational study which included data from a 4-year follow-up of AS patients with heterozygous mutations whose datasets had been included in an analysis of the 2010 database of the European Alport Registry. Using Kaplan-Meier estimates and logrank tests, we prospectively analyzed the updated datasets of 52 of these patients and 13 new datasets (patients added to the Registry after 2011). The effects of therapy, extrarenal symptoms and inheritance pattern on renal outcome were analyzed. The mean prospective follow-up was 46 +/- 10 months, and the mean time on therapy was 8.4 +/- 4.4 (median 7; range 2-18) years. The time from the appearance of the first symptom to diagnosis was 8.1 +/- 14.2 (range 0-52) years. At the time of starting therapy, 5.4 % of patients had an estimated glomerular filtration rate of < 60 ml/min, 67.6 % had proteinuria and 27.0 % had microalbuminuria. Therapeutic strategies included angiotensin-converting enzymer inhibitors (97.1 %), angiotensin receptor antagonists (1 patient), dual therapy (11.8 %) and statins (8.8 %). Among patients included in the prospective dataset, prevented the need for dialysis. Among new patients, no patient at risk for renal failure progressed to the next disease stage after 4 years follow-up; three patients even regressed to a lower stage during therapy. Treatment with blockers of the renin-angiotensin-aldosterone system prevents progressive renal failure in AS patients with heterozygous mutations in the genes causing AS. Considerable numbers of aging AS patients on dialysis may have heterozygous mutations in these genes (present in 1 % of total population) as underlying disease. Hence, greater alertness towards timely diagnosis and therapy has the potential to prevent progressive renal failure in most-if not all-AS patients with heterozygous mutations in the causal genes."],["dc.identifier.doi","10.1007/s00467-016-3452-z"],["dc.identifier.isi","000388976400015"],["dc.identifier.pmid","27402170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43676"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-198X"],["dc.relation.issn","0931-041X"],["dc.title","Prospective study on the potential of RAAS blockade to halt renal disease in Alport syndrome patients with heterozygous mutations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","410"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","186"],["dc.contributor.author","Schminke, Boris"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Bode, Christa"],["dc.contributor.author","Goldring, Mary B."],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-08-20T09:58:00Z"],["dc.date.available","2018-08-20T09:58:00Z"],["dc.date.issued","2016"],["dc.description.abstract","The aim of this study was to investigate the role of laminins and nidogen-2 in osteoarthritis (OA) and their potential to support chondrogenic differentiation. We applied immunohistochemistry, electron microscopy, siRNA, quantitative RT-PCR, Western blot, and proteome analysis for the investigation of cartilage tissue and isolated chondrocytes in three-dimensional culture obtained from patients with late-stage knee OA and nidogen-2 knockout mice. We demonstrate that subunits of laminins appear in OA cartilage and that nidogen-2-null mice exhibit typical osteoarthritic features. Chondrogenic progenitor cells (CPCs) produced high levels of laminin-α1, laminin-α5, and nidogen-2 in their pericellular matrix, and laminin-α1 enhanced collagen type II and reduced collagen type I expression by cultured CPCs. Nidogen-2 increased SOX9 gene expression. Knockdown of nidogen-2 reduced SOX9 expression, whereas it up-regulated RUNX2 expression. This study reveals that the influence of the pericellular matrix on CPCs is important for the expression of the major regulator transcription factors, SOX9 and RUNX2. Our novel findings that laminins and nidogen-2 drive CPCs toward chondrogenesis may help in the elucidation of new treatment strategies for cartilage tissue regeneration."],["dc.identifier.doi","10.1016/j.ajpath.2015.10.014"],["dc.identifier.pmid","26683663"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15413"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1525-2191"],["dc.title","Laminins and Nidogens in the Pericellular Matrix of Chondrocytes: Their Role in Osteoarthritis and Chondrogenic Differentiation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1329"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Tayyeb, Asima; 1School of Biological Sciences, University of the Punjab, Lahore 53700, Pakistan; asima.sbs@pu.edu.pkm"],["dc.contributor.affiliation","Dihazi, Gry H.; 2UMG-Laboratories, Institute for Clinical Chemistry, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; gryhelene.dihazi@med.uni-goettingen.de"],["dc.contributor.affiliation","Tampe, Björn; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Zeisberg, Michael; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Tampe, Desiree; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Hakroush, Samy; 4Department of Pathology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; samy.hakroush@googlemail.com"],["dc.contributor.affiliation","Bührig, Charlotte; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Frese, Jenny; 5Department of Occupational Medicine and Health Safety, Deutsche Post AG, Kölnische Strasse 81, 34117 Kassel, Germany; jenny.frese@med.uni-goettingen.de"],["dc.contributor.affiliation","Serin, Nazli; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Eltoweissy, Marwa; 7Department of Zoology, Faculty of Science, Alexandria University, Alexandria 21568, Egypt; marwaeltoweissy@alexu.edu.eg"],["dc.contributor.affiliation","Müller, Gerhard A.; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Dihazi, Hassan; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.author","Tayyeb, Asima"],["dc.contributor.author","Dihazi, Gry H."],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Bührig, Charlotte"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Serin, Nazli"],["dc.contributor.author","Eltoweissy, Marwa"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Müller, Gerhard A."],["dc.date.accessioned","2022-05-02T08:09:34Z"],["dc.date.available","2022-05-02T08:09:34Z"],["dc.date.issued","2022"],["dc.date.updated","2022-05-05T12:28:41Z"],["dc.description.abstract","Renal Ca2+ reabsorption plays a central role in the fine-tuning of whole-body Ca2+ homeostasis. Here, we identified calreticulin (Calr) as a missing link in Ca2+ handling in the kidney and showed that a shortage of Calr results in mitochondrial disease and kidney pathogenesis. We demonstrated that Calr+/− mice displayed a chronic physiological low level of Calr and that this was associated with progressive renal injury manifested in glomerulosclerosis and tubulointerstitial damage. We found that Calr+/− kidney cells suffer from a disturbance in functionally active calcium stores and decrease in Ca2+ storage capacity. Consequently, the kidney cells displayed an abnormal activation of Ca2+ signaling and NF-κB pathways, resulting in inflammation and wide progressive kidney injury. Interestingly, the disturbance in the Ca2+ homeostasis and signaling in Calr+/− kidney mice cells triggered severe mitochondrial disease and aberrant mitophagy, resulting in a high level of oxidative stress and energy shortage. These findings provide novel mechanistic insight into the role of Calr in kidney calcium handling, function, and pathogenesis."],["dc.description.abstract","Renal Ca2+ reabsorption plays a central role in the fine-tuning of whole-body Ca2+ homeostasis. Here, we identified calreticulin (Calr) as a missing link in Ca2+ handling in the kidney and showed that a shortage of Calr results in mitochondrial disease and kidney pathogenesis. We demonstrated that Calr+/− mice displayed a chronic physiological low level of Calr and that this was associated with progressive renal injury manifested in glomerulosclerosis and tubulointerstitial damage. We found that Calr+/− kidney cells suffer from a disturbance in functionally active calcium stores and decrease in Ca2+ storage capacity. Consequently, the kidney cells displayed an abnormal activation of Ca2+ signaling and NF-κB pathways, resulting in inflammation and wide progressive kidney injury. Interestingly, the disturbance in the Ca2+ homeostasis and signaling in Calr+/− kidney mice cells triggered severe mitochondrial disease and aberrant mitophagy, resulting in a high level of oxidative stress and energy shortage. These findings provide novel mechanistic insight into the role of Calr in kidney calcium handling, function, and pathogenesis."],["dc.identifier.doi","10.3390/cells11081329"],["dc.identifier.pii","cells11081329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107412"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","2073-4409"],["dc.title","Calreticulin Shortage Results in Disturbance of Calcium Storage, Mitochondrial Disease, and Kidney Injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","519"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","20"],["dc.contributor.affiliation","Frese, Jenny; \t\t \r\n\t\t Clinic of Nephrology and Rheumatology, University Medical Center Goettingen, 37075 Goettingen, Germany, jenny.frese@dpdhl.com"],["dc.contributor.affiliation","Kettwig, Matthias; \t\t \r\n\t\t Clinic of Pediatrics and Adolescent Medicine, University Medical Center Goettingen, 37075 Goettingen, Germany, matthias.kettwig@med.uni-goettingen.de"],["dc.contributor.affiliation","Zappel, Hildegard; \t\t \r\n\t\t Clinic of Pediatrics and Adolescent Medicine, University Medical Center Goettingen, 37075 Goettingen, Germany, hzappel@med.uni-goettingen.de"],["dc.contributor.affiliation","Hofer, Johannes; \t\t \r\n\t\t Department of Pediatrics, Pediatrics I, Innsbruck Medical University, 6020 Innsbruck, Austria, Johannes.Hofer@i-med.ac.at"],["dc.contributor.affiliation","Gröne, Hermann-Josef; \t\t \r\n\t\t Department of Cellular and Molecular Pathology, German Cancer Research Center, 69120 Heidelberg, Germany, h.-j.groene@dkfz-heidelberg.de"],["dc.contributor.affiliation","Nagel, Mato; \t\t \r\n\t\t Center for Nephrology and Metabolic Disorders, Molecular Diagnostics, 02943 Weißwasser, Germany, nagel@moldiag.de"],["dc.contributor.affiliation","Sunder-Plassmann, Gere; \t\t \r\n\t\t Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, 1090 Vienna, Austria, Gere.Sunder-Plassmann@meduniwien.ac.at"],["dc.contributor.affiliation","Kain, Renate; \t\t \r\n\t\t Department of Pathology, Medical University of Vienna, 1090 Vienna, Austria, renate.kain@meduniwien.ac.at"],["dc.contributor.affiliation","Neuweiler, Jörg; \t\t \r\n\t\t Institute of Pathology, Kantonsspital, 9007 St. Gallen, Switzerland, joerg.neuweiler@kssg.ch"],["dc.contributor.affiliation","Gross, Oliver; \t\t \r\n\t\t Clinic of Nephrology and Rheumatology, University Medical Center Goettingen, 37075 Goettingen, Germany, gross.oliver@med.uni-goettingen.de"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Kettwig, Matthias"],["dc.contributor.author","Zappel, Hildegard"],["dc.contributor.author","Hofer, Johannes"],["dc.contributor.author","Gröne, Hermann-Josef"],["dc.contributor.author","Nagel, Mato"],["dc.contributor.author","Sunder-Plassmann, Gere"],["dc.contributor.author","Kain, Renate"],["dc.contributor.author","Neuweiler, Jörg"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2019-07-09T11:50:02Z"],["dc.date.available","2019-07-09T11:50:02Z"],["dc.date.issued","2019"],["dc.date.updated","2022-09-05T07:17:34Z"],["dc.description.abstract","Kidney injury due to focal segmental glomerulosclerosis (FSGS) is the most common primary glomerular disorder causing end-stage renal disease. Homozygous mutations in either glomerular basement membrane or slit diaphragm genes cause early renal failure. Heterozygous carriers develop renal symptoms late, if at all. In contrast to mutations in slit diaphragm genes, hetero- or hemizygous mutations in the X-chromosomal COL4A5 Alport gene have not yet been recognized as a major cause of kidney injury by FSGS. We identified cases of FSGS that were unexpectedly diagnosed: In addition to mutations in the X-chromosomal COL4A5 type IV collagen gene, nephrin and podocin polymorphisms aggravated kidney damage, leading to FSGS with ruptures of the basement membrane in a toddler and early renal failure in heterozygous girls. The results of our case series study suggest a synergistic role for genes encoding basement membrane and slit diaphragm proteins as a cause of kidney injury due to FSGS. Our results demonstrate that the molecular genetics of different players in the glomerular filtration barrier can be used to evaluate causes of kidney injury. Given the high frequency of X-chromosomal carriers of Alport genes, the analysis of genes involved in the organization of podocyte architecture, the glomerular basement membrane, and the slit diaphragm will further improve our understanding of the pathogenesis of FSGS and guide prognosis of and therapy for hereditary glomerular kidney diseases."],["dc.identifier.doi","10.3390/ijms20030519"],["dc.identifier.pmid","30691124"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15841"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59686"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Kidney Injury by Variants in the COL4A5 Gene Aggravated by Polymorphisms in Slit Diaphragm Genes Causes Focal Segmental Glomerulosclerosis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13"],["dc.bibliographiccitation.journal","Matrix Biology"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Rubel, Diana"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Martin, Maria"],["dc.contributor.author","Leibnitz, Alexander"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Eckes, Beate"],["dc.contributor.author","Müller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2021-06-01T10:49:46Z"],["dc.date.available","2021-06-01T10:49:46Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.matbio.2014.01.006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86405"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0945-053X"],["dc.title","Collagen receptors integrin alpha2beta1 and discoidin domain receptor 1 regulate maturation of the glomerular basement membrane and loss of integrin alpha2beta1 delays kidney fibrosis in COL4A3 knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]