Elmar Endl

Publications (77) View all

• Article: Einsatz von Nanopartikeln in der Augenheilkunde

  I. Hahn, P. Heiduschka, E. Endl, N. Eter
  [show abstract] [hide abstract]
  ABSTRACT: Die Nanotechnologie, also die Herstellung und der Einsatz von Strukturen und Werkzeugen in der Größenordnung von einigen wenigen bis 100nm, ist auf dem Weg zu einer Schlüsseltechnologie des 21.Jahrhunderts. Ein wichtiges Element für die Herstellung von Nanopartikeln ist Gold. Goldnanopartikel lassen sich in Größe und Gestalt maßschneidern und chemisch modifizieren. Bei ersten Untersuchungen zeigte sich, dass sie physiologisch unbedenklich sind. Ein potenzielles Anwendungsgebiet ist die neovaskuläre altersbedingte Makuladegeneration. In die sich neu bildenden Blutgefäße eingebrachte Goldnanopartikel geeigneter Dimension können durch einen Laser gezielt erhitzt werden, wodurch diese Blutgefäße selektiv zerstört werden. An kultivierten Endothelzellen konnte dieses Prinzip bereits demonstriert werden. Nanotechnology, the manufacture and use of structures and implements of around a few 100nm in size, is becoming a key technology of the twenty-first century. An important element for the manufacture of nanoparticles is gold. Gold nanoparticles can be custom made and chemically modified in their size and form. Initial investigations have shown that they are physiologically non-hazardous. A potential application is in neovascular age-related macular degeneration. Gold nanoparticles of suitable dimensions introduced into newly forming blood vessels can be targeted and heated which selectively destroys these blood vessels. This principle has already been demonstrated in cultivated endothelial cells. SchlüsselwörterNanotechnologie–Goldnanopartikel–Altersbedingte Makuladegeneration–Endothelzellen–Neovaskularisation KeywordsNanotechnology–Gold particles–Age-related macular degeneration–Endothelial cells–Neovascularization
  Der Ophthalmologe 04/2012; 108(9):863-868. · 0.62 Impact Factor
• Article: [Use of nanoparticles in ophthalomology].

  I Hahn, P Heiduschka, E Endl, N Eter
  [show abstract] [hide abstract]
  ABSTRACT: Nanotechnology, the manufacture and use of structures and implements of around a few 100 nm in size, is becoming a key technology of the twenty-first century. An important element for the manufacture of nanoparticles is gold. Gold nanoparticles can be custom made and chemically modified in their size and form. Initial investigations have shown that they are physiologically non-hazardous. A potential application is in neovascular age-related macular degeneration. Gold nanoparticles of suitable dimensions introduced into newly forming blood vessels can be targeted and heated which selectively destroys these blood vessels. This principle has already been demonstrated in cultivated endothelial cells.
  Der Ophthalmologe 07/2011; 108(9):863-8. · 0.62 Impact Factor
• Article: Basic molecular fingerprinting of immature cerebellar cortical inhibitory interneurons and their precursors.

  A Glassmann, S Topka, L Wang-Eckardt, S Anders, G Weisheit, E Endl, A Zimmer, K Schilling
  [show abstract] [hide abstract]
  ABSTRACT: While the development of cerebellar granule and Purkinje neurons has been extensively studied, little is known about the developmental mechanisms that lead to the generation and diversification of inhibitory GABAergic interneurons of the cerebellar cortex. To address this issue, we compared gene expression in complete, early postnatal murine cerebella to that in cerebella from which immature inhibitory interneurons and their precursors had been stripped based on their expression of green fluorescent protein (GFP) from the Pax2 locus. We identified some 300 candidate genes selectively enriched within immature cerebellar cortical inhibitory interneurons and/or their precursors, many of which were also expressed in their adult descendants and/or the embryonic cerebellar ventricular epithelium that gives rise to these cells. None of the genes identified, among them Tcfap2alpha, Tcfap2beta, Lbxcor1 and Lbx1, was cell-type specific. Rather, gene expression, and also splicing, changed dynamically during development and rather reflects stage of differentiation than lineage. Consistently, cluster analysis of transcriptional regulators and genes specific for adult cerebellar GABAergic cells does not suggest a hierarchical lineage relationship or an early commitment of subtypes of cerebellar cortical inhibitory interneurons. Together, these data support the notion that diversification of cerebellar inhibitory interneurons is highly regulative and subject to local signaling to postmigratory precursors.
  Neuroscience 01/2009; 159(1):69-82. · 3.38 Impact Factor
• Source

  Available from: Elmar Endl

  Article: Insulin-like growth factor-1 receptor acts as a growth regulator in synovial sarcoma.

  N Friedrichs, J Küchler, E Endl, A Koch, J Czerwitzki, P Wurst, D Metzger, J H Schulte, M I Holst, L C Heukamp, O Larsson, S Tanaka, A Kawai, E Wardelmann, R Buettner, T Pietsch, W Hartmann
  [show abstract] [hide abstract]
  ABSTRACT: Synovial sarcomas account for 5-10% of all soft tissue sarcomas and the majority of synovial sarcomas display characteristic t(X;18) translocations that result in enhanced transcription of the insulin-like growth factor-2 (IGF-2) gene. IGF-2 is an essential fetal mitogen involved in the pathogenesis of different tumours, leading to cellular proliferation and inhibition of apoptosis. Here we asked whether activation of IGF signalling is of functional importance in synovial sarcomas. We screened human synovial sarcomas for expression of IGF-2 and the phosphorylated IGF-1 receptor (IGF-1R), which mainly mediates the proliferative and anti-apoptotic effects of IGF-2. Since both the phosphatidylinositol 3'-kinase (PI3K)-AKT pathway and the MAPK signalling cascade are known to be involved in the transmission of IGF-1R signals, expression of phosphorylated (p)-AKT and p-p44/42 MAPK was additionally assessed. All tumours expressed IGF-2 and 78% showed an activated IGF-1R. All tumours were found to express p-AKT and 92% showed expression of activated p44/42 MAPK. To analyse the functional and potential therapeutic relevance of IGF-1R signalling, synovial sarcoma cell lines were treated with the IGF-1R inhibitor NVP-AEW541. Growth was impaired by the IGF-1R antagonist, which was consistently accompanied by a dose-dependent reduction of phosphorylation of AKT and p44/42 MAPK. Functionally, inhibition of the receptor led to increased apoptosis and diminished mitotic activity. Concurrent exposure of selected cells to NVP-AEW541 and conventional chemotherapeutic agents resulted in positive interactions. Finally, synovial sarcoma cell migration was found to be dependent on signals transmitted by the IGF-1R. In summary, our data show that the IGF-1R might represent a promising therapeutic target in synovial sarcomas.
  The Journal of Pathology 08/2008; 216(4):428-39. · 6.32 Impact Factor
• Article: Restoration of SHIP activity in a human leukemia cell line downregulates constitutively activated phosphatidylinositol 3-kinase/Akt/GSK-3beta signaling and leads to an increased transit time through the G1 phase of the cell cycle.

  S Horn, E Endl, B Fehse, M M Weck, G W Mayr, M Jücker
  [show abstract] [hide abstract]
  ABSTRACT: The inositol 5-phosphatase SHIP (SHIP-1) is a negative regulator of signal transduction in hematopoietic cells and targeted disruption of SHIP in mice leads to a myeloproliferative disorder. We analyzed the effects of SHIP on the human leukemia cell line Jurkat in which expression of endogenous SHIP protein is not detectable. Restoration of SHIP expression in Jurkat cells with an inducible expression system caused a 69% reduction of phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) and a 65% reduction of Akt kinase activity, which was associated with reduced phosphorylation of glycogen synthase kinase 3beta (GSK-3beta) (Ser-9) without changing the phosphorylation of Bad (Ser-136), FKHR (Ser-256) or MAPK (Thr-202/Tyr-204). SHIP-expressing Jurkat cells showed an increased transit time through the G1 phase of the cell cycle, but SHIP did not cause a complete cell cycle arrest or apoptosis. Extension of the G1 phase was associated with an increased stability of the cell cycle inhibitor p27(Kip1) and reduced phosphorylation of the retinoblastoma protein Rb at serine residue 780. Our data indicate that restoration of SHIP activity in a human leukemia cell line, which has lost expression of endogenous SHIP, downregulates constitutively activated phosphatidylinositol 3-kinase/Akt/GSK-3beta signaling and leads to an increased transit time through the G1 phase of the cell cycle.
  Leukemia 12/2004; 18(11):1839-49. · 9.56 Impact Factor