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","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"]]