Jakubiczka-Smorag, Joanna Matylda

[["dc.bibliographiccitation.firstpage","616"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","627"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Cordasic, Nada"],["dc.contributor.author","Panesar, Julian"],["dc.contributor.author","Buchholz, Bjoern"],["dc.contributor.author","Jacobi, Johannes"],["dc.contributor.author","Hartner, Andrea"],["dc.contributor.author","Klanke, Bernd"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Burzlaff, Nicolai"],["dc.contributor.author","Heinze, Eva"],["dc.contributor.author","Warnecke, Christina"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Willam, Carsten"],["dc.contributor.author","Tsao, Philip S."],["dc.contributor.author","Eckardt, Kai-Uwe"],["dc.contributor.author","Amann, Kerstin"],["dc.contributor.author","Hilgers, Karl F."],["dc.date.accessioned","2018-11-07T10:26:33Z"],["dc.date.available","2018-11-07T10:26:33Z"],["dc.date.issued","2017"],["dc.description.abstract","Chronic kidney disease (CKD) is associated with increased risk and worse prognosis of cardiovascular disease, including peripheral artery disease. An impaired angiogenic response to ischemia may contribute to poor outcomes of peripheral artery disease in patients with CKD. Hypoxia inducible factors (HIF) are master regulators of angiogenesis and therefore represent a promising target for therapeutic intervention. To test this we induced hind-limb ischemia in rats with CKD caused by 5/6 nephrectomy and administered two different treatments known to stabilize HIF protein in vivo: carbon monoxide and a pharmacological inhibitor of prolyl hydroxylation 2-(1-chloro-4-hydroxyisoquinoline-3-carboxamido) acetate (ICA). Expression levels of proangiogenic HIF target genes (Vegf, Vegf-r1, Vegf-r2, Ho-1) were measured by qRT-PCR. Capillary density was measured by CD31 immunofluorescence staining and HIF expression was evaluated by immunohistochemistry. Capillary density in ischemic skeletal muscle was significantly lower in CKD animals compared to sham controls. Rats with CKD showed significantly lower expression of HIF and all measured pro-angiogenic HIF target genes, including VEGF. Both HIF stabilizing treatments rescued HIF target gene expression in animals with CKD and led to significantly higher ischemia-induced capillary sprouting compared to untreated controls. ICA was effective regardless of whether it was administered before or after induction of ischemia and led to a HIF expression in skeletal muscle. Thus, impaired ischemia-induced angiogenesis in rats with CKD can be improved by HIF stabilization, even if started after onset of ischemia."],["dc.identifier.doi","10.1016/j.kint.2016.09.028"],["dc.identifier.isi","000394921400016"],["dc.identifier.pmid","27927598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43067"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.title","Hypoxia inducible factor stabilization improves defective ischemia-induced angiogenesis in a rodent model of chronic kidney disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","813"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Human Genetics"],["dc.bibliographiccitation.lastpage","826"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Santamaria-Araujo, Jose Angel"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Kumar, Avadh"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Schwarz, Guenter"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Reiss, Jochen"],["dc.contributor.author","Smorag, Lukasz"],["dc.date.accessioned","2018-11-07T10:12:30Z"],["dc.date.available","2018-11-07T10:12:30Z"],["dc.date.issued","2016"],["dc.description.abstract","Molybdenum cofactor (MoCo) deficiency is a rare, autosomal-recessive disorder, mainly caused by mutations in MOCS1 (MoCo deficiency type A) or MOCS2 (MoCo deficiency type B) genes; the absence of active MoCo results in a deficiency in all MoCo-dependent enzymes. Patients with MoCo deficiency present with neonatal seizures, feeding difficulties, severe developmental delay, brain atrophy and early childhood death. Although substitution therapy with cyclic pyranopterin monophosphate (cPMP) has been successfully used in both Mocs1 knockout mice and in patients with MoCo deficiency type A, there is currently no Mocs2 knockout mouse and no curative therapy for patients with MoCo deficiency type B. Therefore, we generated and characterized a Mocs2-null mouse model of MoCo deficiency type B. Expression analyses of Mocs2 revealed a ubiquitous expression pattern; however, at the cellular level, specific cells show prominent Mocs2 expression, e.g., neuronal cells in cortex, hippocampus and brainstem. Phenotypic analyses demonstrated that Mocs2 knockout mice failed to thrive and died within 11 days after birth. None of the tested MoCo-dependent enzymes were active in Mocs2-deficient mice, leading to elevated concentrations of purines, such as hypoxanthine and xanthine, and non-detectable levels of uric acid in the serum and urine. Moreover, elevated concentrations of S-sulfocysteine were measured in the serum and urine. Increased levels of xanthine resulted in bladder and kidney stone formation, whereas increased concentrations of toxic sulfite triggered neuronal apoptosis. In conclusion, Mocs2-deficient mice recapitulate the severe phenotype observed in humans and can now serve as a model for preclinical therapeutic approaches for MoCo deficiency type B."],["dc.identifier.doi","10.1007/s00439-016-1676-4"],["dc.identifier.isi","000377364300012"],["dc.identifier.pmid","27138983"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40249"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-1203"],["dc.relation.issn","0340-6717"],["dc.title","Mouse model for molybdenum cofactor deficiency type B recapitulates the phenotype observed in molybdenum cofactor deficient patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","Suppl_1"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Dannert, Angelika"],["dc.contributor.author","Schellinger, Isabel N"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Mattern, Karin"],["dc.contributor.author","Petzold, Anne"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Raaz, Uwe"],["dc.date.accessioned","2020-12-10T18:37:54Z"],["dc.date.available","2020-12-10T18:37:54Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1161/atvb.38.suppl_1.678"],["dc.identifier.eissn","1524-4636"],["dc.identifier.issn","1079-5642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77134"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Abstract 678: microRNA 146a Reduces Activity of Matrix-Metalloproteinases in the Context of Arterial Stiffness"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]