Girgert, Rainer

[["dc.bibliographiccitation.firstpage","440"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","NEUROENDOCRINOLOGY LETTERS"],["dc.bibliographiccitation.lastpage","444"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Bartsch, C."],["dc.contributor.author","Hill, S. M."],["dc.contributor.author","Kreienberg, Rolf"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T10:34:30Z"],["dc.date.available","2018-11-07T10:34:30Z"],["dc.date.issued","2003"],["dc.description.abstract","OBJECTIVES: Detection of the antiestrogenic effect of melatonin on various breast cancer cell lines and its dependence of the differential expression of estrogen receptors (ERalpha and ERbeta) and melatonin receptors (mt1 and RZRalpha,). SETTING AND DESIGN: Dose-response curves of estradiol were determined in 6 different breast cancer cell lines using a colorimetric proliferation assay in the absence or presence of various melatonin concentrations. METHODS: In order to detect the minor growth inhibitory effect of melatonin, a simple yet novel approach was employed: instead of incubating cells at single estradiol-concentrations at increasing melatonin levels, breast cancer cells were grown in microwell-plates for 4 days at increasing concentrations of estradiol (10(-12) M - 10(-10) M) in the absence or presence of melatonin (10(-9) M - 10(-8) M). Cell number was determined using Alamar blue and colorimetry, RT-PCR was performed for the expression of ERalpha, ERbeta, RZRalpha and mt1. RESULTS: Melatonin at concentrations of 10(-9) M and 5x10(-9) M shifted the dose-response curves of estradiol to higher concentrations. Responsiveness to melatonin depended on expression of ERalpha but not on ERbeta. mRNA of ERbeta was not detectable in the breast cancer cell lines used. Only small amounts of mt1 transcripts were detectable in MCF-7 cells of one source. In MCF-7 cells transfected with the mt1 gene and in an ovarian cancer cell line mt1 was expressed at significant levels. RZRalpha was expressed in all tested cell lines at different amounts. CONCLUSION: The growth of all ERalpha-positive breast cancer cell lines can be inhibited by melatonin. The effect in most cell lines is weak yet clearly reproducible. RZRalpha clearly contributes to the growth inhibitory effect of melatonin."],["dc.identifier.isi","000187882100012"],["dc.identifier.pmid","15073572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44887"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Maghira & Maas Publications"],["dc.relation.issn","0172-780X"],["dc.title","Tracking, the elusive antiestrogenic effect of melatonin: A new methodological approach"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","334"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Journal of Gynecological Cancer"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:31:09Z"],["dc.date.available","2018-11-07T08:31:09Z"],["dc.date.issued","2009"],["dc.description.abstract","Effects of electromagnetic fields (EMFs) on the incidence of breast cancer (BC) have been proposed by a number of epidemiological studies. The molecular mechanism of the impact of EMFs on cells is not yet clear, although changes in gene expression have been reported in various cellular systems. In this investigation, the interference of low-frequency EMFs with the plasminogen activator system was examined in BC cells. MCF-7 BC cells from 2 different sources were exposed to highly homogeneous 50-Hz EMFs. Changes in gene expression were analyzed by reverse transcriptase-polymerase chain reaction. In MCF-7 cells exposed to 1.2 mu T ENT expression of the urokinase plasminogen activator gene and of plasminogen-activator inhibitor-1 was markedly increased. The expression of the receptor for urokinase plasminogen activator was only marginally increased in I of the 2 tested cell lines and expression of the tissue plasminogen activator was at least slightly down-regulated in BC cells exposed to EMFs. EMFs may be able to increase the metastatic potential of breast tumors. The use of our newly established exposure system for EMFs may allow us to study the signaling processes involved in the induction of a metastatic phenotype of breast cancer cells."],["dc.identifier.doi","10.1111/IGC.0b013e31819f53ec"],["dc.identifier.isi","000266976600006"],["dc.identifier.pmid","19407555"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17055"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1048-891X"],["dc.title","Exposure of MCF-7 Breast Cancer Cells to Electromagnetic Fields Up-Regulates the Plasminogen Activator System"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","199"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Breast Cancer Research and Treatment"],["dc.bibliographiccitation.lastpage","205"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T09:08:33Z"],["dc.date.available","2018-11-07T09:08:33Z"],["dc.date.issued","2012"],["dc.description.abstract","Triple-negative breast cancers lack estrogen receptor alpha (ER alpha), progesterone receptor, and do not overexpress human epidermal growth factor receptor 2 (Her-2). They are neither susceptible to endocrine therapy nor to a therapy using the anti-Her-2 antibody, trastuzumab. Therefore, an efficient targeted therapy is warranted. Triple-negative breast tumors frequently express membrane bound estrogen receptor G-protein coupled receptor (GPR30). As proof of principle, we analyzed the consequences of a knock-down of GPR30 expression on the growth regulation of triple-negative breast cancer cell lines. Cells of triple-negative breast cancer cell lines were transfected with siRNA against GPR30 or control siRNA, and cell growth was stimulated either with 10(-9) M 17 beta-estradiol or 10(-6) M 4-hydroxytamoxifen. Cell proliferation was measured using Alamar blue staining. Activation of c-Src and epidermal growth factor (EGF)-receptor was assessed using western blot. Expression of c-fos was quantified by reverse transcription polymerase chain reaction. Seven days after transfection with siRNA, GPR30 mRNA in triple-negative breast cancer cell lines MDA-MB-435 and HCC1806 was reduced by 74 and 90%, respectively. 10(-8) M 17 beta-estradiol enhanced proliferation of MDA-MB-435 to 129.6 +/- A 5.4% of control (p < 0.05) and HCC1806 to 156.9 +/- A 15.4% of control (p < 0.05), respectively. 10(-6) M 4-hydroxytamoxifen increased cell number of MDA-MB-435 to 121.0 +/- A 6.9% of control (p < 0.05) and HCC1806 to 124.5 +/- A 12.1% of control (n.s.), respectively. This increased proliferation by the two estrogenic compounds was completely prevented by knock-down of GPR30 expression in both cell lines. In control cells, activity of Src kinase was increased 3-fold by estradiol and 3.8-fold using 4-hydroxytamoxifen. Transactivation of the EGF-receptor was similarly increased in both cell lines by 17 beta-estradiol and 4-hydroxytamoxifen. Both compounds increased c-fos expression 1.5- and 3.1-fold, respectively. Knock-down of GPR30 expression completely abolished activation of all these signaling pathways responsible for enhanced proliferation. A pharmacological inhibition of GPR30 by specific small molecular inhibitors might prove to be an appropriate targeted therapy of triple-negative breast cancer in the future."],["dc.identifier.doi","10.1007/s10549-012-1968-x"],["dc.identifier.isi","000306437500018"],["dc.identifier.pmid","22290080"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8116"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26060"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0167-6806"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Inactivation of GPR30 reduces growth of triple-negative breast cancer cells: possible application in targeted therapy"],["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.issue","3"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Schimming, H."],["dc.contributor.author","Kreienberg, Rolf"],["dc.contributor.author","Girgert, Rainer"],["dc.date.accessioned","2018-11-07T10:50:33Z"],["dc.date.available","2018-11-07T10:50:33Z"],["dc.date.issued","2004"],["dc.format.extent","109"],["dc.identifier.doi","10.1016/S1359-6349(04)90796-3"],["dc.identifier.isi","000202990100211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48684"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","1359-6349"],["dc.title","Antiproliferative activity of tamoxifen on MCF-7 breast cancer cells is modulated by weak electromagnetic field exposure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Oncology Letters"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, G�nter"],["dc.contributor.author","Gr�ndker, Carsten"],["dc.date.accessioned","2020-12-10T18:47:38Z"],["dc.date.available","2020-12-10T18:47:38Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3892/ol.2018.8521"],["dc.identifier.eissn","1792-1082"],["dc.identifier.issn","1792-1074"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78831"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Inhibition of growth hormone receptor by Somavert reduces expression of GPER and prevents growth stimulation of triple‑negative breast cancer by 17β‑estradiol"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","169"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bioelectromagnetics"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T11:16:21Z"],["dc.date.available","2018-11-07T11:16:21Z"],["dc.date.issued","2008"],["dc.description.abstract","Breast cancer is the most common malignancy of women in Western societies. The increasing exposure to electromagnetic fields has been suspected to contribute to the rising incidence of breast cancer in industrialized Countries. The majority of breast tumors is treated with the partial antiestrogen tamoxifen. Most tumors become resistant to tamoxifen in the course of treatment resulting in treatment failure. Electromagnetic fields reduce the efficacy of tamoxifen similar to tamoxifen resistance. In this study we investigated the mechanism by which electromagnetic fields influence the sensitivity to tamoxifen. In cells exposed to 1.2 mu T of a 50 Hz electromagnetic field gene expression of cofactors of the estrogen receptors was compared to sham exposed cells. Using a gene array technology several cofactors were found to be differentially expressed. The expression of the coactivators, SRC-I and AIB 1, and of two corepressors, N-Cor and SMRT, was quantified by RT-PCR. Both coactivators were expressed more strongly in the exposed cells while the expression of two corepressors decreased. The RNA analysis was confirmed by Western blots. The contradirectional changes in gene expression of coactivators and corepressors by electromagnetic fields results in a lower sensitivity to tamoxifen. Electromagnetic fields may contribute to the induction of tamoxifen resistance in vivo. Bioelectromagnetics 29:169-176, 2008. (C) 2007 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/bem.20387"],["dc.identifier.isi","000254479100002"],["dc.identifier.pmid","18027843"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54564"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0197-8462"],["dc.title","Electromagnetic fields alter the expression of estrogen receptor cofactors in breast cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.lastpage","10"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Martin, Maria"],["dc.contributor.author","Kruegel, Jenny"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Temme, Johanna"],["dc.contributor.author","Eckes, Beate"],["dc.contributor.author","Müller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2019-07-09T11:52:48Z"],["dc.date.available","2019-07-09T11:52:48Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Integrins are important cellular receptors for collagens. Within the glomerulus, podocytes regulate the integrity of the glomerular basement membrane (GBM) by sensing the presence of collagen and regulating collagen IV synthesis. The present study evaluates the role of integrin a2 (ITGA2) in cell-matrix interaction. Methods and Results: ITGA2-deficient mice had normal renal function but moderate proteinuria and enhanced glomerular and tubulointerstitial matrix deposition. Electron microscopy demonstrated irregular podocyte-matrix interaction, causing pathological protrusions towards the urinary (podocyte) side of the GBM. These characteristic subepithelial bulges mimic the renal phenotype of mice, which are deficient in another collagen receptor, discoidin domain receptor (DDR)1. Using immunogold staining, ITGA2 expression was found to localize to the basolateral site of the podocyte foot processes. ITGA2-deficient mice overexpressed transforming growth factor (TGF)b and connective tissue growth factor (CTGF) compared with wild-type mice. Using in situ hybridization, tubular cells were found to be the primary site of TGFb synthesis and podocytes the source of CTGF in ITGA2- deficient mice. Conclusion: These findings support our hypothesis that both these collagen receptors (ITGA2 and DDR1) play a similar role within the kidney. Further, cell-matrix interaction via collagen receptors seems to be crucial for maintenance of normal GBM architecture and function. Targeting collagen receptors such as ITGA2 might be a new form of treatment for progressive fibrotic diseases."],["dc.identifier.doi","10.1186/1755-1536-3-19"],["dc.identifier.fs","575629"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60281"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/6905 but duplicate"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Integrin a2-deficient mice provide insights into specific functions of collagen receptors in the kidney"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","American Journal of Hypertension"],["dc.bibliographiccitation.lastpage","361"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Gross, O."],["dc.contributor.author","Girgert, R."],["dc.contributor.author","Rubel, D."],["dc.contributor.author","Temme, J."],["dc.contributor.author","Theissen, S."],["dc.contributor.author","Muller, G.-A."],["dc.date.accessioned","2021-06-01T10:50:32Z"],["dc.date.available","2021-06-01T10:50:32Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1038/ajh.2010.231"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86697"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1941-7225"],["dc.relation.issn","0895-7061"],["dc.title","Renal Protective Effects of Aliskiren Beyond Its Antihypertensive Property in a Mouse Model of Progressive Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","237"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bioelectromagnetics"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:44:20Z"],["dc.date.available","2018-11-07T08:44:20Z"],["dc.date.issued","2010"],["dc.description.abstract","The growth of estrogen-receptor positive breast cancer cells is inhibited by the pineal gland hormone, melatonin. Concern has been raised that power-line frequency and microwave electromagnetic fields (EMEs) could reduce the efficiency of melatonin on breast cancer cells. In this study we investigated the impact of EMIT's on the signal transduction of the high-affinity receptor MT1 M parental MCF-7 cells and MCF-7 cells transfected with the MT1 gene. The binding of the cAMP-responsive element binding (CREB) protein to a promoter sequence of BRCA-1 after stimulation with melatonin was analyzed by a gel-shift assay and the expression of four estrogen-responsive genes was measured in sham-exposed breast cancer cells and cells exposed to a sinusoidal 50Hz EMF of 1.2 mu T for 48 h. In sham-exposed cells, binding of CREB to the promoter of BRCA-1 was increased by estradiol and subsequently diminished by treatment with melatonin. In cells exposed to 1.2 mu T, 50Hz. EMF. binding of CREB was almost completely omitted. Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level. In contrast, in breast cancer cells transfected with MT1 exposed to 1.2 mu T of the 50Hz EMF, the expression of p53 and c-myc increased significantly after melatonin treatment but for p21(WAF). the increase was not significant. These results convincingly prove the negative effect of EMF on the antiestrogenic effect of melatonin in breast cancer cells. Bioelectromagnetics 31:237-245, 2010. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/bem.20554"],["dc.identifier.isi","000276052600008"],["dc.identifier.pmid","19882681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20177"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0197-8462"],["dc.title","Signal Transduction of the Melatonin Receptor MT1 Is Disrupted in Breast Cancer Cells by Electromagnetic Fields"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1012"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","1019"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Rubel, D."],["dc.contributor.author","Stock, J."],["dc.contributor.author","Ciner, A."],["dc.contributor.author","Hiller, H."],["dc.contributor.author","Girgert, R."],["dc.contributor.author","Muller, G.-A."],["dc.contributor.author","Gross, O."],["dc.date.accessioned","2021-06-01T10:51:21Z"],["dc.date.available","2021-06-01T10:51:21Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1093/ndt/gft434"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86983"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1460-2385"],["dc.relation.issn","0931-0509"],["dc.title","Antifibrotic, nephroprotective effects of paricalcitol versus calcitriol on top of ACE-inhibitor therapy in the COL4A3 knockout mouse model for progressive renal fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]