Ahmad, Shakil

[["dc.bibliographiccitation.firstpage","11471"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","International journal of clinical and experimental pathology"],["dc.bibliographiccitation.lastpage","11479"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Moriconi, Federico"],["dc.date.accessioned","2019-07-10T08:12:06Z"],["dc.date.available","2019-07-10T08:12:06Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: The liver plays a key role in iron homeostasis during injury and hypoxia. Methods: For induction of liver injury, thioacetamide (TAA) was administered intraperitoneally to male Sprague Dawley rats. Animals were sacrificed at 0, 1, 3, 6, 12, 24, 48, 72 and 96 h. Serum, liver, spleen and heart tissues were collected from control and TAA-treated rats. Tissue sections were prepared for immunohistochemical studies. Nuclear and cytoplasmic proteins were isolated for Western blot analysis. Results: Hypoxia inducible factor (HIF)-1α and ED1 positive cells accumulated around the portal field and the interlobular space within 12 hours after TAA administration. Accordingly, Western blot analysis of liver tissue showed an early increase of HIF1α followed by a decrease at 48 h to 96 h. For Erythropoietin (EPO), as well as for HIF1- and -2α, a time-dependent translocation was observed from the cytoplasmic to the nuclear compartment. Conclusion: Our data suggest that the TAA-induced acute liver damage generates HIF-1α dependent rescue mechanisms with translocation of EPO from the cytoplasmic to the nuclear compartment. Enhanced iron transport into the liver could be necessary for increased metabolic activities during repair processes."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60864"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","1936-2625"],["dc.rights.access","openAccess"],["dc.subject","Thioacetamide (TAA); acute phase injury; hypoxia inducible factor (HIF); erythropoietin (EPO)"],["dc.subject.ddc","610"],["dc.title","Mediators of hypoxia in a rat model of sterile-induced acute liver injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","3891"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","19"],["dc.contributor.affiliation","Ahmad, Shakil; \t\t \r\n\t\t Department of Gastroenterology and Endocrinology, University Hospital, Georg-August University Goettingen, 37075 Goettingen, Germany, shakil.ahmad@med.uni-goettingen.de\t\t \r\n\t\t Department of Cardiology and Pneumology, University Hospital, Georg-August University Goettingen, 37075 Goettingen, Germany, shakil.ahmad@med.uni-goettingen.de"],["dc.contributor.affiliation","Ramadori, Giuliano; \t\t \r\n\t\t Department of Gastroenterology and Endocrinology, University Hospital, Georg-August University Goettingen, 37075 Goettingen, Germany, giulianoramadori@gmail.com"],["dc.contributor.affiliation","Moriconi, Federico; \t\t \r\n\t\t Department of Gastroenterology and Endocrinology, University Hospital, Georg-August University Goettingen, 37075 Goettingen, Germany, federicomoriconi@hotmail.it\t\t \r\n\t\t GastroCentro, Via Trevano 38, 6900 Lugano, Switzerland, federicomoriconi@hotmail.it"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Moriconi, Federico"],["dc.date.accessioned","2019-07-09T11:49:38Z"],["dc.date.available","2019-07-09T11:49:38Z"],["dc.date.issued","2018"],["dc.date.updated","2022-09-06T16:43:55Z"],["dc.description.abstract","Kupffer cells are professional phagocytes of the liver clearing bacteria from portal blood. Their clearance capacity, however, can be overwhelmed, transforming them into critical mediators of hepatic-injury. We investigated the consequences of selective Kupffer cell-overload by intraperitoneally administering pyrogen-free gadolinium chloride (GdCl3) or Zymosan into rats and into endotoxin-resistant mice (C3H/HeJ). The number of myeloperoxidase-positive (MPO+) cells increased at 3 h mainly around the portal vessel after both GdCl3 and Zymosan treatment. Simultaneously, GdCl3 administration reduced detectability of ED-1+ (but not ED-2) cells near the portal vessel. Serum chemokine (C-X-C motif) ligand 1 (CXCL-1), CXCL-2 and chemokine (C-C motif) ligand 2 (CCL-2) showed a peak at 3 h after both treatment regimens although at a higher extent after Zymosan administration. Accordingly, CXCL-1, CXCL-5 and CCL-2 gene expression in the liver was up-regulated after GdCl3 treatment at 3 h. After Zymosan administration a significant up-regulation of CXCL-1, CXCL-2, CXCL-10, CCL-2, CCL-3 and CCL-20 gene expression in liver at 3 h was observed. After Zymosan administration intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) gene expression was up-regulated in rat liver tissue. In C3H/HeJ mice both treatment regimens up-regulated CCL-2 and ICAM-1 gene expression after 3 h and down-regulated platelet endothelial cell adhesion molecule 1 (PECAM-1) gene expression. In conclusion, phagocytosis overload of Kupffer cells causes induction of several CXC, CC-chemokines, upregulation of “positive” adhesion molecule gene expression, down-regulation of the “negative” adhesion molecule PECAM-1 and a recruitment of neutrophil granulocytes in the portal area of the liver of treated rats and mice mainly in close contact to the liver macrophages."],["dc.identifier.doi","10.3390/ijms19123891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15730"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59596"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Modulation of Chemokine- and Adhesion-Molecule Gene Expression and Recruitment of Neutrophil Granulocytes in Rat and Mouse Liver after a Single Gadolinium Chloride or Zymosan Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]