Siggelkow, Heide

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","JBMR Plus"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Wilde, Deborah"],["dc.contributor.author","Wilken, Lara"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Heppner, Christina"],["dc.contributor.author","Chavanon, Mira‐Lynn"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2021-06-01T10:50:47Z"],["dc.date.available","2021-06-01T10:50:47Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jbm4.10245"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17136"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86788"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2473-4039"],["dc.relation.issn","2473-4039"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The HPQ—Development and First Administration of a Questionnaire for Hypoparathyroid Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","331"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Journal of Molecular Histology"],["dc.bibliographiccitation.lastpage","341"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Tezval, Mohammad"],["dc.contributor.author","Tezval, Hossein"],["dc.contributor.author","Dresing, Klaus"],["dc.contributor.author","Stuermer, Ewa Klara"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Stuermer, Klaus Michael"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2018-11-07T11:23:52Z"],["dc.date.available","2018-11-07T11:23:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Urocortin-1 (UCN) a corticotropin releasing-factor (CRF) related peptide, has been found to be expressed in many different tissues like the central nervous system, the cardiovascular system, adipose tissue, and skeletal muscle. The effects of UCN are mediated via stimulation of CRF-receptors 1 and 2 (CRFR1 and 2, CRFR's) with a high affinity for CRFR2. It has been shown that the CRF-related peptides and CRFR's are involved in the regulation of stress-related endocrine, autonomic and behavioural responses. Using immunocytochemistry, immunohistochemistry and RT-PCR, we now can show the differentiation dependent expression of UCN mRNA and peptide in human mesenchymal progenitor cells (MSCs) directed to the osteoblastic phenotype for the first time. UCN expression was down regulated by TGF-beta and BMP-2 in the early proliferation phase of osteoblast development, whereas dexamethasone (dex) minimally induced UCN gene expression during matrix maturation after 24 h stimulation. Stimulation of MSCs for 28 days with ascorbate/beta-glycerophosphate (asc/bGp) induced UCN gene expression at day 14. This effect was prevented when using 1,25-vitamin D3 or dex in addition. There was no obvious correlation to osteocalcin (OCN) gene expression in these experiments. In MSCs from patients with metabolic bone disease (n = 9) UCN gene expression was significantly higher compared to MSCs from normal controls (n = 6). Human MSCs did not express any of the CRFR's during differentiation to osteoblasts. Our results indicate that UCN is produced during the development of MSCs to osteoblasts and differentially regulated during culture as well as by differentiation factors. The expression is maximal between proliferation and matrix maturation phase. However, UCN does not seem to act on the osteoblast itself as shown by the missing CRFR's. Our results suggest new perspectives on the role of urocortin in human skeletal tissue in health and disease."],["dc.identifier.doi","10.1007/s10735-009-9244-z"],["dc.identifier.isi","000275443300002"],["dc.identifier.pmid","19949969"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4160"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56279"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1567-2379"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Differentiation dependent expression of urocortin's mRNA and peptide in human osteoprogenitor cells: influence of BMP-2, TGF-beta-1 and dexamethasone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","P1"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","P19"],["dc.bibliographiccitation.volume","181"],["dc.contributor.author","Bollerslev, Jens"],["dc.contributor.author","Schalin-Jäntti, Camilla"],["dc.contributor.author","Rejnmark, Lars"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Morreau, Hans"],["dc.contributor.author","Thakker, Rajesh"],["dc.contributor.author","Sitges-Serra, Antonio"],["dc.contributor.author","Cetani, Filomena"],["dc.contributor.author","Marcocci, Claudio"],["dc.contributor.author","Guistina, Andrea"],["dc.contributor.author","Van Hul, Wim"],["dc.contributor.author","Amrein, Karin"],["dc.contributor.author","Sikjaer, Tanja"],["dc.contributor.author","Hindie, Elif"],["dc.contributor.author","Vamvakidis, Kyriakos"],["dc.contributor.author","Corbetta, Sabrina"],["dc.contributor.author","Balaia, Zhanna"],["dc.contributor.author","Astor, Marianne"],["dc.contributor.author","Makay, Ozer"],["dc.contributor.author","Newey, Paul"],["dc.contributor.author","Hannan, Fadil"],["dc.contributor.author","Rolighed, Lars"],["dc.contributor.author","Appelman-Dijkstra, Natasha"],["dc.contributor.author","Wicke, Corrina"],["dc.contributor.author","Pilz, Stefan"],["dc.contributor.author","Saponaro, Federica"],["dc.contributor.author","Vestergard, Peter"],["dc.date.accessioned","2020-12-10T18:42:39Z"],["dc.date.available","2020-12-10T18:42:39Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1530/EJE-19-0316"],["dc.identifier.eissn","1479-683X"],["dc.identifier.issn","0804-4643"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16464"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78039"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Unmet therapeutic, educational and scientific needs in parathyroid disorders: Consensus Statement from the first European Society of Endocrinology Workshop (PARAT)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1342"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cellular Biochemistry"],["dc.bibliographiccitation.lastpage","1355"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Ponce, M. L."],["dc.contributor.author","Koelling, Sebastian"],["dc.contributor.author","Kluever, A."],["dc.contributor.author","Heinemann, D. E. H."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Frosch, Karl-Heinz"],["dc.contributor.author","Schuetze, N."],["dc.contributor.author","Hufner, A."],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2018-11-07T11:13:34Z"],["dc.date.available","2018-11-07T11:13:34Z"],["dc.date.issued","2008"],["dc.description.abstract","Knowledge of the basic mechanisms controlling osteogenesis and adipogenesis might provide new insights into the prevention of osteoporosis and age-related osteopenia. With the help of magnetic cell sorting and fluorescence activated cell sorting (FACS), osteoblastic subpopulations of mesenchymal progenitor cells were characterized. Alkaline phosphatase (AP) negative cells expressed low levels of osteoblastic and adipocytic markers. AP positive cells expressed adipocytic markers more strongly than the AP negative cell populations, thus suggesting that committed osteoblasts exhibit a greater adipogenic potential. AP negative cells differentiated to the mature osteoblastic phenotype, as demonstrated by increased AP-activity and osteocalcin secretion under standard osteogenic culture conditions. Surprisingly, this was accompanied by increased expression of adipocytic gene markers such as peroxisome proliferator-activated receptor-gamma 2, lipoprotein lipase and fatty acid binding protein. The induction of adipogenic markers was suppressed by transforming growth factor-beta 1 (TGF-beta 1) and promoted by bone morphogenetic protein 2 (BMP-2). Osteogenic culture conditions including BMP-2 induced both the formation of mineralized nodules and cytoplasmic lipid vacuoles. Upon immunogold electron microscopic analysis, osteoblastic and adipogenic marker proteins were detectable in the same cell. Our results suggest that osteogenic and adipogenic differentiation in human mesenchymal progenitor cells might not be exclusively reciprocal, but rather, a parallel event until late during osteoblast development."],["dc.identifier.doi","10.1002/jcb.21711"],["dc.identifier.isi","000257567300018"],["dc.identifier.pmid","18286543"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6248"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53928"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0730-2312"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Coexpression of osteogenic and adipogenic differentiation markers in selected subpopulations of primary human mesenchymal progenitor cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Riemann, Annika; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.affiliation","Blaschke, Martina; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.affiliation","Jauho-Ghadimi, Annukka; 2MVZ Endokrinologikum Göttingen, 37075 Göttingen, Germany; mari.jauho-ghadimi@amedes-group.com"],["dc.contributor.affiliation","Siggelkow, Heide; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.affiliation","Gollisch, Katja Susanne Claudia; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.author","Riemann, Annika"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Jauho-Ghadimi, Annukka"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Gollisch, Katja Susanne Claudia"],["dc.date.accessioned","2022-08-03T14:32:55Z"],["dc.date.available","2022-08-03T14:32:55Z"],["dc.date.issued","2022-07-24"],["dc.date.updated","2022-08-03T13:41:59Z"],["dc.description.abstract","Non-alcoholic fatty liver disease (NAFLD) is a common yet little recognized health problem in women with polycystic ovary syndrome (PCOS). In a retrospective setting, we investigated the effects of metformin treatment on the hepatic steatosis index (HSI) as a readily available biomarker panel for NAFLD. HSI values of >36 are considered to be highly suggestive for NAFLD. In our cohort, HSI values indicating NAFLD were found in 60/81 (74.1%) women at baseline. The mean HSI improved significantly after the metformin treatment from 43.2 ± 1.0 to 41.0 ± 1.1. Subgroup analyses of non-obese (body mass index (BMI) < 30 kg/m2), obese (BMI 30–35 kg/m2) and very obese (BMI > 35 kg/m2) women yielded mean baseline HSI values of 35.5 ± 4.5, 41.2 ± 2.7 and 51.2 ± 4.7, respectively. A significant improvement in the HSI of 1.5 ± 2.1 was observed after metformin treatment in non-obese women but not in the obese subgroups. The data suggest a new aspect of metformin treatment in non-obese PCOS patients, namely, a possible improvement in NAFLD. This study highlighted hepatic steatosis as a common comorbidity in PCOS patients that can severely affect their long-term health, and therefore, deserves more attention in the management of PCOS patients."],["dc.identifier.doi","10.3390/jcm11154294"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112604"],["dc.language.iso","en"],["dc.relation.eissn","2077-0383"],["dc.rights","CC BY 4.0"],["dc.title","Metformin Improves the Hepatic Steatosis Index in Non-Obese Patients with Polycystic Ovary Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","JBMR Plus"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Wilken, Lara"],["dc.contributor.author","Wilde, Deborah"],["dc.contributor.author","Heppner, Christina"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2022-04-01T10:01:30Z"],["dc.date.available","2022-04-01T10:01:30Z"],["dc.date.issued","2022"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1002/jbm4.10586"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105677"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2473-4039"],["dc.relation.issn","2473-4039"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","The Influence of Conventional Treatment on Symptoms and Complaints in Patients With Chronic Postsurgical Hypoparathyroidism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","159"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Endocrinology"],["dc.bibliographiccitation.lastpage","168"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Clarke, Bart L."],["dc.contributor.author","Germak, John"],["dc.contributor.author","Marelli, Claudio"],["dc.contributor.author","Chen, Kristina"],["dc.contributor.author","Dahl‐Hansen, Helen"],["dc.contributor.author","Glenister, Elizabeth"],["dc.contributor.author","Bent‐Ennakhil, Nawal"],["dc.contributor.author","Judge, Davneet"],["dc.contributor.author","Mycock, Katie"],["dc.contributor.author","Bollerslev, Jens"],["dc.date.accessioned","2020-01-14T10:41:54Z"],["dc.date.accessioned","2021-10-27T13:22:06Z"],["dc.date.available","2020-01-14T10:41:54Z"],["dc.date.available","2021-10-27T13:22:06Z"],["dc.date.issued","2020"],["dc.description.abstract","OBJECTIVE: To address knowledge gaps regarding burdens associated with not adequately controlled chronic hypoparathyroidism. DESIGN: Global patient and caregiver survey. STUDY POPULATIONS: Patients with chronic hypoparathyroidism not adequately controlled on conventional therapy and their caregivers. MEASUREMENTS: Health-related quality of life (HRQoL) and health status were evaluated using the 36-item Short Form version 2 (SF-36 v2.0) and Five-Level EuroQoL 5 Dimensions (EQ-5D-5L) instruments, respectively. Hypoparathyroidism-associated symptoms were assessed by a disease-specific Hypoparathyroidism Symptom Diary and caregiver burden via the Modified Caregiver Strain Index (MCSI). RESULTS: Data were obtained from 398 patients and 207 caregivers. Patients' self-rated hypoparathyroidism-related symptom severity was none (3%), mild (32%), moderate (53%) or severe (12%). Per the Hypoparathyroidism Symptom Diary, patients reported moderate, severe or very severe symptoms of physical fatigue (73%), muscle cramps (55%), heaviness in limbs (55%) and tingling (51%) over a 7-day recall period. Impacts (rated 'somewhat' or 'very much') were reported by 84% of patients for ability to exercise, 78% for sleep, 75% for ability to work and 63% for family relationships. Inverse relationships were observed between patient self-rated overall symptom severity and HRQoL and health status assessment scores-the greater the symptom severity, the lower the SF-36 and EQ-5D-5L scores. Caregiver burden increased with patient self-rated symptom severity: none, 1.7 MCSI; mild, 5.4 MCSI; moderate, 9.5 MCSI; and severe, 12.5 MCSI. CONCLUSION: Patients with not adequately controlled hypoparathyroidism reported substantial symptoms and impacts. Greater patient symptom severity was associated with decreased patient HRQoL and health status assessments and increased caregiver burden."],["dc.identifier.doi","10.1111/cen.14128"],["dc.identifier.eissn","1365-2265"],["dc.identifier.isbn","31721256"],["dc.identifier.issn","0300-0664"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92068"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1365-2265"],["dc.relation.issn","1365-2265"],["dc.relation.issn","0300-0664"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Burden of illness in not adequately controlled chronic hypoparathyroidism: Findings from a 13‐country patient and caregiver survey"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1483"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Endocrine Connections"],["dc.bibliographiccitation.lastpage","1492"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kahlert, Elin"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Freiberg, Clemens"],["dc.contributor.author","Janssen, Onno E"],["dc.contributor.author","Stahnke, Nikolaus"],["dc.contributor.author","Strik, Domenika"],["dc.contributor.author","Merkel, Martin"],["dc.contributor.author","Mann, Alexander"],["dc.contributor.author","Liesenkötter, Klaus-Peter"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2020-12-10T18:42:39Z"],["dc.date.available","2020-12-10T18:42:39Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1530/EC-19-0418"],["dc.identifier.eissn","2049-3614"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78038"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Deficient knowledge in adult Turner syndrome care as an incentive to found Turner centers in Germany"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","JBMR Plus"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Wilde, Deborah"],["dc.contributor.author","Wilken, Lara"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Heppner, Christina"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2021-06-01T10:50:50Z"],["dc.date.available","2021-06-01T10:50:50Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jbm4.10368"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86799"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2473-4039"],["dc.relation.issn","2473-4039"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Quantification of Symptom Load by a Disease‐Specific Questionnaire HPQ 28 and Analysis of Associated Biochemical Parameters in Patients With Postsurgical Hypoparathyroidism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Advances in Clinical and Experimental Medicine"],["dc.bibliographiccitation.lastpage","56"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Koepp, Regine"],["dc.contributor.author","Cortis, Julia"],["dc.contributor.author","Komrakova, Marina"],["dc.contributor.author","Schieker, Matthias"],["dc.contributor.author","Hempel, Ute"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2020-12-10T18:42:47Z"],["dc.date.available","2020-12-10T18:42:47Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND: Crohn´s disease (CD) is associated with a higher prevalence of osteoporosis. The pathogenesis of bone affliction remains controversial, especially if inflammatory cytokines or glucocorticoid therapy are the main contributors. In postmenopausal osteoporosis, bone resorption is induced by IL-6, IL-1β and TNF-α. In contrast, in children with CD, IL-6 exclusively decreased bone formation without affecting bone resorption. OBJECTIVES: The objective of this study was to further clarify the pathophysiology of bone affliction in adult patients with CD with the use of an osteoblast and osteoclast cell model. MATERIAL AND METHODS: Inflammatory cytokines IL-6, IL-1β, and TNF-α were measured in adult CD patients' serum. Mean values of these cytokines were applied with or without dexamethasone to the human cell line SCP-1 (osteoblastic cell model). Also, the effect of cytokines on primary human osteoclast differentiation and activity was determined. RESULTS: The combined cytokine application increased the receptor activator of NF-κB ligand/osteoprotegerin (RANKL/OPG) ratio 2-fold after 2 and 14 days. Additional application of dexamethasone to SCP-1 cells further increased the RANKL/OPG ratio 3-fold, but decreased IL-6 and IL-1β expression to 10% and 50%, respectively. TNF-α expression was maximally suppressed to 16% by dexamethasone in the presence of cytokines. In osteoclasts, the combined cytokine treatment decreased expression of characteristic genes to approx. 30%, while increasing osteoclast resorption activity to 148%. In addition, a cytokine stimulated osteoblast cell culture-generated supernatant stimulated osteoclast resorption activity by 170%. CONCLUSIONS: Our results suggest that IL-6, IL-1β, and TNF-α only in combination induced osteoclaststimulating activity represented by the RANKL/OPG ratio in osteoblasts. Dexamethasone further increased this effect in osteoblasts, while decreasing cytokine expression. The results in osteoclasts support a direct and osteoblast-mediated effect on bone resorption. Our in vitro results differentiate for the first time the effect of cytokines on bone turnover as measured in adult CD patients from the additional dexamethasone effect on osteoblasts as part of the pathophysiology of osteoporosis."],["dc.identifier.doi","10.17219/acem/67561"],["dc.identifier.issn","1899-5276"],["dc.identifier.pmid","29521042"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15197"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78085"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.issn","1899-5276"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","IL-6, IL-1β, and TNF-α only in combination influence the osteoporotic phenotype in Crohn’s patients via bone formation and bone resorption"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]