Forest remnants in the hills of the southern Vienna basin (Lower Austria)

Die vorliegende Arbeit beschäftigt sich mit der Erfassung und Beschreibung von elf Waldresten im südlich der Donau liegenden Teil des Wiener Beckens. Das Untersuchungsgebiet ist durch von Löss bedeckte Schotterterrassen geprägt. Die Waldreste wurden floristisch erfasst und syntaxonomisch bearbeitet. Zusätzlich wurde in den Franziszäischen Kataster von 1820 Einsicht genommen, um genauere Informationen über die damaligen Nutzungsformen der heutigen Waldflächen zu erhalten. Die Eichen- Hainbuchenwälder wurden in das Polygonato latifolii-Carpinetum, die Eichenwälder großenteils in das Euphorbio angulatae-Quercetum eingereiht. Innerhalb dieser Assoziation wurden vier Ausbildungen ausgewiesen (degradiert, frisch, mäßig trocken und trocken). Eine Aufnahme wurde zum Lithospermo purpurocaerulei-Quercetum pubescentis gestellt. Drei Aufnahmen aus Beständen, die deutlich durch die Robinie überprägt sind, wurden als Balloto-Robinietum klassifiziert. Das Areal dieser Eichen- und Eichen-Hainbuchenwälder ist altes Siedlungsgebiet und wird seit Jahrhunderten (z.T. Jahrtausenden) genutzt, weshalb der Wald nur noch in Form von Fragmenten erhalten ist. Weiters sind neophytische Baumarten wie die Robinie und der Götterbaum ein Problem für den Fortbestand dieser Wälder, da sie die natürliche Artenzusammensetzung der Bestände verändern.This paper describes 11 forest remnants in the southern part of the Vienna basin. The Vienna basin is a fracture zone between the Alps in the west and the Carpathians in the east. The study area is characterised by loess-covered terraces. The forests are floristically described and syntaxonomically classified. Additional information was collected from the land survey of 1820 known as the “Franziszäischer Kataster”, in order to characterize former land use of the forests. The oak-hornbeam forests of the study area were classified as Polygonato latifolii-Carpinetum, the oak forests mainly as Euphorbio angulatae-Quercetum. Within this association, four subtypes were noted (degraded, mesic, moderately dry and dry). One relevé was classified as Lithospermo purpurocaerulei-Quercetum pubescentis. Three relevés that were highly affected by Robinia pseudacacia were classified as Balloto-Robinietum. The oak- and oak-hornbeam forests lie in an old settlement area and thus have been used for many centuries. The forest is thus present in only small fragments. There is also a problem with neophytes like Robinia and Ailanthus. These trees are a danger for the continuity and the species composition of the forest remnants

Phenobarbital induces alterations in the proteome of hepatocytes and mesenchymal cells of rat livers.

Preceding studies on the mode of action of non-genotoxic hepatocarcinogens (NGCs) have concentrated on alterations induced in hepatocytes (HCs). A potential role of non-parenchymal liver cells (NPCs) in NGC-driven hepatocarcinogenesis has been largely neglected so far. The aim of this study is to characterize NGC-induced alterations in the proteome profiles of HCs as well as NPCs. We chose the prototypic NGC phenobarbital (PB) which was applied to male rats for a period of 14 days. The livers of PB-treated rats were perfused by collagenase and the cell suspensions obtained were subjected to density gradient centrifugation to separate HCs from NPCs. In addition, HCs and NPC isolated from untreated animals were treated with PB in vitro. Proteome profiling was done by CHIP-HPLC and ion trap mass spectrometry. Proteome analyses of the in vivo experiments showed many of the PB effects previously described in HCs by other methods, e.g. induction of phase I and phase II drug metabolising enzymes. In NPCs proteins related to inflammation and immune regulation such as PAI-1 and S100-A10, ADP-ribosyl cyclase 1 and to cell migration such as kinesin-1 heavy chain, myosin regulatory light chain RLC-A and dihydropyrimidinase-related protein 1 were found to be induced, indicating major PB effects on these cells. Remarkably, in vitro treatment of HCs and NPCs with PB hardly reproduced the proteome alterations observed in vivo, indicating differences of NGC induced responses of cells at culture conditions compared to the intact organism. To conclude, the present study clearly demonstrated that PB induces proteome alterations not only in HCs but also in NPCs. Thus, any profound molecular understanding on the mode of action of NGCs has to consider effects on cells of the hepatic mesenchyme

Autonomous inhibition of apoptosis correlates with responsiveness of colon carcinoma cell lines to ciglitazone.

Colorectal cancer is a leading cause of mortality worldwide. Resistance to therapy is common and often results in patients succumbing to the disease. The mechanisms of resistance are poorly understood. Cells basically have two possibilities to survive a treatment with potentially apoptosis-inducing substances. They can make use of their existing proteins to counteract the induced reactions or quickly upregulate protective factors to evade the apoptotic signal. To identify protein patterns involved in resistance to apoptosis, we studied two colorectal adenocarcinoma cell lines with different growth responses to low-molar concentrations of the thiazolidinedione Ciglitazone: HT29 cells underwent apoptosis, whereas SW480 cells increased cell number. Fluorescence detection and autoradiography scans of 2D-PAGE gels were performed in both cell lines to assess protein synthesis and turnover, respectively. To verify the data we performed shotgun analysis using the same treatment procedure as in 2D-experiments. Biological functions of the identified proteins were mainly associated with apoptosis regulation, chaperoning, intrinsic inflammation, and DNA repair. The present study suggests that different growth response of two colorectal carcinoma cell lines after treatment with Ciglitazone results from cell-specific protein synthesis and differences in protein regulation

Functional Classification of Cellular Proteome Profiles Support the Identification of Drug Resistance Signatures in Melanoma Cells

Drug resistance is a major obstacle in melanoma treatment. Recognition of specific resistance patterns, the understanding of the patho-physiology of drug resistance, and identification of remaining options for individual melanoma treatment would greatly improve therapeutic success. We performed mass spectrometry-based proteome profiling of A375 melanoma cells and HeLa cells characterized as sensitive to cisplatin in comparison to cisplatin resistant M24met and TMFI melanoma cells. Cells were fractionated into cytoplasm, nuclei and secretome and the proteome profiles classified according to Gene Ontology. The cisplatin resistant cells displayed increased expression of lysosomal as well as Ca²⁺ ion binding and cell adherence proteins. These findings were confirmed using Lysotracker Red staining and cell adhesion assays with a panel of extracellular matrix proteins. To discriminate specific survival proteins, we selected constitutively expressed proteins of resistant M24met cells which were found expressed upon challenging the sensitive A375 cells. Using the CPL/MUW proteome database, the selected lysosomal, cell adherence and survival proteins apparently specifying resistant cells were narrowed down to 47 proteins representing a potential resistance signature. These were tested against our proteomics database comprising more than 200 different cell types/cell states for its predictive power. We provide evidence that this signature enables the automated assignment of resistance features as readout from proteome profiles of any human cell type. Proteome profiling and bioinformatic processing may thus support the understanding of drug resistance mechanism, eventually guiding patient tailored therapy

Proteome profiling in IL-1β and VEGF-activated human umbilical vein endothelial cells delineates the interlink between inflammation and angiogenesis

<div><p>Endothelial cells represent major effectors in inflammation and angiogenesis, processes that drive a multitude of pathological states such as atherosclerosis and cancer. Both inflammation and angiogenesis are interconnected with each other in the sense that many pro-inflammatory proteins possess proangiogenic properties and vice versa. To elucidate this interplay further, we present a comparative proteome study of inflammatory and angiogenic activated endothelial cells. HUVEC were stimulated with interleukin 1-β and VEGF, respectively. Cultured primary cells were fractionated into secreted, cytoplasmic and nuclear protein fractions and processed for subsequent LC-MS/MS analysis. Obtained protein profiles were filtered for fraction-specific proteins to address potential cross fractional contamination, subjected to comparative computational biology analysis (GO-Term enrichment analysis, weighted gene co-expression analysis) and compared to published mRNA profiles of IL-1β respectively VEGF stimulated HUVEC. GO Term enrichment analysis and comparative pathway analysis revealed features such as NOD and NfkB signaling for inflammatory activated HUVEC and VEGF and ErB signaling for VEGF-activated HUVEC with potential crosstalk via map kinases MAP2K2. Weighted protein co-expression network analysis revealed several potential hub genes so far not associated with driver function in inflammation or angiogenesis such as HSPG2, ANXA3, and GPI. “Classical” inflammation or angiogenesis markers such as IL6, CXCL8 or CST1 were found in a less central position within the co-expression networks. In conclusion, this study reports a framework for the computational biology based analysis of proteomics data applied to cytoplasmic, nucleic and extracellular fractions of quiescent, inflammatory and angiogenic activated HUVEC. Novel potential hub genes relevant for these processes were successfully identified.</p></div

ClueGO analysis of the fractions of HUVEC treated with 10ng/mL IL-1β and HUVEC treated with 10ng/mL VEGF with untreated HUVEC as control.

<p>(A) cytoplasm fraction, (B) nucleic compartment, (C) extracellular fraction. Color depicts the fraction of induced proteins in IL-1β-treated HUVEC (red) and VEGF-treated HUVEC (blue). Node size depicts the p-value of the pathway. A summary of the analysis is provided in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0179065#pone.0179065.s002" target="_blank">S2 Table</a>.</p