Siggelkow, Heide

[["dc.bibliographiccitation.artnumber","S0960076021000431"],["dc.bibliographiccitation.firstpage","105850"],["dc.bibliographiccitation.journal","The Journal of Steroid Biochemistry and Molecular Biology"],["dc.bibliographiccitation.volume","210"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Koepp, Regine"],["dc.contributor.author","Streit, Frank"],["dc.contributor.author","Beismann, Johannes"],["dc.contributor.author","Manthey, Georg"],["dc.contributor.author","Seitz, Mark-Tilmann"],["dc.contributor.author","Kragl, Angelique"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2021-07-05T15:00:19Z"],["dc.date.available","2021-07-05T15:00:19Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.jsbmb.2021.105850"],["dc.identifier.pii","S0960076021000431"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87797"],["dc.language.iso","en"],["dc.notes.intern","DOI Import DOI-Import GROB-441"],["dc.relation.issn","0960-0760"],["dc.title","The rise in expression and activity of 11β-HSD1 in human mesenchymal progenitor cells induces adipogenesis through increased local cortisol synthesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","582"],["dc.bibliographiccitation.issue","09"],["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.lastpage","595"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Komrakova, Marina"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Ponce, Maria Laura"],["dc.contributor.author","Klüver, Anne"],["dc.contributor.author","Köpp, Regine"],["dc.contributor.author","Hüfner, Michael"],["dc.contributor.author","Schieker, Matthias"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2021-04-14T08:23:08Z"],["dc.date.available","2021-04-14T08:23:08Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1055/a-1084-3888"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80806"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1439-3646"],["dc.relation.issn","0947-7349"],["dc.title","Decreased Expression of the Human Urea Transporter SLC14A1 in Bone is Induced by Cytokines and Stimulates Adipogenesis of Mesenchymal Progenitor Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Endocrine Abstracts"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Stamm, Niklas"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Gruszendorf, Martin"],["dc.date.accessioned","2019-10-14T07:04:38Z"],["dc.date.available","2019-10-14T07:04:38Z"],["dc.date.issued","2019"],["dc.description.abstract","Patients (pts) with hypoparathyroidism (HypoPT) are at risk to develop renal failure possibly caused by hypercalciuria and nephrocalcinosis. We retrospectively evaluated the data of 711 Patients with HypoPT in 3 endocrine centres in Germany. Methods: Records of 711 pts with HypoPT were reviewed. Patients were predominantly female (n=592, male: n=119; age 50.9±14.1 years, range 12 – 99 years). The following parameters were documented during treatment and follow-up (MW 52±40.9 months, time range 2–334 months): medication, calcium in serum and urine, phosphate, calcium-phosphate-product (CPP), glomerular filtration rate (GFR) calculated by CKD-EPI formula. Results: Of these 711 pts. 29 had idiopathic HypoPT, 10 HypoPT after parathyroidectomy, 669 after thyroid operation. At first visit 4.0% of pts <40 years, 11.1% in the age group 40–59, 28.4% in the age group 60–69, and 49.0% in pts >69 years had a GFR < 60 ml/min. At the last visit no worsening of renal function was observed (GFR < 60 ml/min in 5.9% <40 years, 9.8% in the age group 40–59, 17.1% in the age group 60–69, 36.0% >69 years). An elevated CPP > 55 mg2/dl2 was found in 25 pts (3.5%). In these pts the proportion of GFR < 60 ml/min was 33.5% compared to 21.1% of those with normal CPP. In comparison of the therapeutic strategies pts treated exclusively with dihydrotachysterol renal function was the lowest (n=46; mean GFR 70.2±26.2 ml/min). In pts treated with calcitriol and calcium (n=226) mean GFR was better than in all other treatment groups (84.9±20.9). Conclusion: We saw no worsening of renal function in a large cohort of patients with HypoPT during 4 years of therapy. High CPP was associated with lower GFR. Different treatment strategies of HypoPT seem to affect kidney function."],["dc.identifier.doi","10.1530/endoabs.63.OC1.5"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62487"],["dc.language.iso","en"],["dc.relation.issn","1479-6848"],["dc.title","Renal function in 711 patients with hypoparathyroidism during more than 4 years of therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","953034"],["dc.bibliographiccitation.journal","Frontiers in Bioengineering and Biotechnology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kragl, Angelique"],["dc.contributor.author","Schoon, Janosch"],["dc.contributor.author","Tzvetkova, Ana"],["dc.contributor.author","Wenzel, Christoph"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Böcker, Wolfgang"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Tzvetkov, Mladen V."],["dc.date.accessioned","2022-10-04T10:22:04Z"],["dc.date.available","2022-10-04T10:22:04Z"],["dc.date.issued","2022"],["dc.description.abstract","Exogenous glucocorticoids increase the risk for osteoporosis, but the role of endogenous glucocorticoids remains elusive. Here, we describe the generation and validation of a loss- and a gain-of-function model of the cortisol producing enzyme 11β-HSD1 (\n HSD11B1\n ) to modulate the endogenous glucocorticoid conversion in SCP-1 cells — a model for human mesenchymal stem cells capable of adipogenic and osteogenic differentiation. CRISPR-Cas9 was successfully used to generate a cell line carrying a single base duplication and a 5 bp deletion in exon 5, leading to missense amino acid sequences after codon 146. These inactivating genomic alterations were validated by deep sequencing and by cloning with subsequent capillary sequencing. 11β-HSD1 protein levels were reduced by 70% in the knockout cells and cortisol production was not detectable. Targeted chromosomal integration was used to stably overexpress\n HSD11B1\n . Compared to wildtype cells,\n HSD11B1\n overexpression resulted in a 7.9-fold increase in\n HSD11B1\n mRNA expression, a 5-fold increase in 11β-HSD1 protein expression and 3.3-fold increase in extracellular cortisol levels under adipogenic differentiation. The generated cells were used to address the effects of 11β-HSD1 expression on adipogenic and osteogenic differentiation. Compared to the wildtype,\n HSD11B1\n overexpression led to a 3.7-fold increase in mRNA expression of lipoprotein lipase\n (LPL)\n and 2.5-fold increase in lipid production under adipogenic differentiation. Under osteogenic differentiation,\n HSD11B1\n knockout led to enhanced alkaline phosphatase (ALP) activity and mRNA expression, and\n HSD11B1\n overexpression resulted in a 4.6-fold and 11.7-fold increase in mRNA expression of Dickkopf-related protein 1\n (DKK1)\n and\n LPL\n , respectively. Here we describe a\n HSD11B1\n loss- and gain-of-function model in SCP-1 cells at genetic, molecular and functional levels. We used these models to study the effects of endogenous cortisol production on mesenchymal stem cell differentiation and demonstrate an 11β-HSD1 dependent switch from osteogenic to adipogenic differentiation. These results might help to better understand the role of endogenous cortisol production in osteoporosis on a molecular and cellular level."],["dc.identifier.doi","10.3389/fbioe.2022.953034"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114580"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","2296-4185"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Effects of HSD11B1 knockout and overexpression on local cortisol production and differentiation of mesenchymal stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Bone"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Peiffer, K."],["dc.contributor.author","Tzvetkov, Mladen Vassilev"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Kopp, R."],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2018-11-07T08:28:58Z"],["dc.date.available","2018-11-07T08:28:58Z"],["dc.date.issued","2009"],["dc.format.extent","S307"],["dc.identifier.doi","10.1016/j.bone.2009.03.568"],["dc.identifier.isi","000266348600267"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16541"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","36th European Symposium on Calcified Tissues"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","8756-3282"],["dc.title","Evidence for expression of siRNA directed against RUNX2 mRNA by psilencer in mesenchymal progenitor cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]