Kamrowski-Kruck, Heike

[["dc.bibliographiccitation.firstpage","18"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Loffler, B. M."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","von Ahsen, N."],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T09:12:33Z"],["dc.date.available","2018-11-07T09:12:33Z"],["dc.date.issued","2001"],["dc.description.abstract","Astrocytes are known to possess an effective endothelin (ET) eliminatory system which involves astrocytic ETA and ETB receptors and may become particularly relevant under pathophysiological conditions. The present study has therefore been designed to explore the effect of standardized hypoxia on extracellular concentrations of endothelin-1 (ET-1) and on endothelin-converting enzyme (ECE) activity in primary rat astrocytes genetically (sl/sl) or experimentally (dexamethasone) deficient in ETB receptors. The results revealed (1) a hypoxia-mediated decrease of extracellular ET-1 in wildtype astrocytes (+/+) that was not observed in ETB-deficient (sl/sl) cultures; (2) an ET receptor antagonist-induced increase in ET-1 in the media of both genotypes with further elevation upon hypoxia in +/+ cultures only; (3) augmentation of the dexamethasone-induced increase in extracellular ET-1 by hypoxia in +/+, but not in sl/sl cultures; (4) synergistic reduction of ETB gene transcription by hypoxia and dexamethasone; and (5) significant increases in endothelin-converting enzyme activity in the presence of hypoxia. To conclude, hypoxia stimulates astrocytic release of mature ET-1, This stimulation is (over)compensated for by increased ET-1 binding to functional ETB receptors. ETB deficiency, whether genetic or experimentally induced, impairs elimination of extracellular (C) 2001 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.1036"],["dc.identifier.isi","000167958400003"],["dc.identifier.pmid","11284016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26960"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Role of the astrocytic ETB receptor in the regulation of extracellular endothelin-1 during hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","957"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Neurochemical Research"],["dc.bibliographiccitation.lastpage","969"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Schilling, L."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Hahn, A."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T10:42:23Z"],["dc.date.available","2018-11-07T10:42:23Z"],["dc.date.issued","2000"],["dc.description.abstract","We characterized the time-course, intensity of expression and cellular origin of components of the endothelin (ET) system in the rat brain after a standardized neurotrauma (cryogenic lesion of the parietal cortex). ET mRNAs were expressed at sham level after neurotrauma, whereas immunoreactivity for ET-1 was enhanced in glia and endothelium of the lesioned hemisphere and both hippocampi. The number of ET-3 positive mononuclear cells in the lesion perimeter increased starting at 24h after injury. At 48h after neurotrauma, ET-receptor immunoreactivity was increased in astrocytes. In basilar artery endothelium, ETB-immunoreactivity was reduced at 48h to 72h recovering at 7 days whereas ETA-receptor and ET-peptide immunoreactivities were not altered. In summary, neurotrauma leads to a multicellular stimulation of endothelins in the brain along with a delayed selective loss of vascular ETB-receptors. These changes seem to be posttranscriptional and cell type specific. They favor vasoconstriction increasing the risk of late vasospasm and ischemia."],["dc.identifier.doi","10.1023/A:1007552408463"],["dc.identifier.isi","000088734500008"],["dc.identifier.pmid","10959492"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46784"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Kluwer Academic/plenum Publ"],["dc.relation.issn","0364-3190"],["dc.title","Differential glial and vascular expression of endothelins and their receptors in rat brain after neurotrauma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3485"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Neuroreport"],["dc.bibliographiccitation.lastpage","3488"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Heyer, A."],["dc.contributor.author","Unzicker, C."],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T11:00:45Z"],["dc.date.available","2018-11-07T11:00:45Z"],["dc.date.issued","2000"],["dc.description.abstract","The potential of erythropoietin (EPO) to reduce hypoxia-induced cell death has been investigated in 5-day-old primary cultures of rat postnatal hippocampal neurons. Application of EPO (100 pM) at the start of hypoxia resulted in a significant reduction of neuronal death (33.0 +/- 7.5% in cells incubated with EPO vs 56.75 +/- 7.3% in non-treated cells; n = 4, p < 0.021). Similiar results were obtained upon application of cycloheximide (CHX; 1 M) simultaneously with hypoxia (34.75 +/- 5.6% vs 56.75 +/- 7.3% with and without CHX, respectively, n = 4, p < 0.035), indicating that hypoxia-induced neuronal death is an active, protein synthesis-dependent process. Both, EPO and EPO receptor (EPOR) were found to; be expressed after hypoxia in hippocampal neurons in vitro and in vivo. These results demonstrate for the first time that EPO can reverse hypoxia-induced neuronal death when applied simultaneously with the hypoxic stimulus. NeuroReport 11:3485-3488 (C) 2000 Lippincott Williams & Wilkins."],["dc.identifier.doi","10.1097/00001756-200011090-00017"],["dc.identifier.isi","000165301600017"],["dc.identifier.pmid","11095504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50997"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0959-4965"],["dc.title","Survival of hippocampal neurons in culture upon hypoxia: effect of erythropoietin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]