Frese, Jenny

[["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"]]