80 research outputs found
Dataset on the activation of Mueller cells through macrophages upon hypoxia in the retina
The dataset presented in this article complements the article entitled "Myeloid cells contribute indirectly to VEGF expression upon hypoxia via activation of Mueller cells" (C. Nuernberg, N. Kociok, C. Brockmann, T. Lischke, S. Crespo-Garcia, N. Reichhart, S. Wolf, R. Baumgrass, S.A. Eming, S. Beer-Hammer, and A.M. Joussen). This complementary dataset provides further insight into the experimental validation of the VEGF(fl/fl) LysMCre (here named VEGF(mcko)) knockout model used in the main article through genomic and quantitative Real-Time PCR in various murine tissues as well as additional flow cytometry data and immunohistochemical stainings. By providing these data, we aim to enable researcher to reproduce and critically analyze our data
Etoposide upregulates survival favoring sphingosine-1-phosphate in etoposide-resistant retinoblastoma cells
Improved knowledge of retinoblastoma chemotherapy resistance is needed to raise treatment efficiency. The objective of this study was to test whether etoposide alters glucosyl-ceramide, ceramide, sphingosine, and sphingosine-1-phosphate (sphingosine-1-P) levels in parental retinoblastoma cells (WERI Rb1) or their etoposide-resistant subclones (WERI EtoR). WERI Rb1 and WERI EtoR were incubated with 400 ng/ml etoposide for 24 h. Levels of glucosyl-ceramides, ceramides, sphingosine, sphingosine-1-P were detected by Q-TOF mass spectrometry. Statistical analysis was done by ANOVA followed by Tukey post-hoc test (p 0.2). Both cell lines upregulate pro-apoptotic sphingosine after etoposide incubation, but only WERI EtoR produces additional survival favorable sphingosine-1-P. These data may suggest a role of sphingosine-1-P in retinoblastoma chemotherapy resistance, although this seems not to be the only resistance mechanism
An unforeseen polymorph of coronene by the application of magnetic fields during crystal growth
Contains fulltext :
158779.pdf (publisher's version ) (Open Access
Knock-Down of Cathepsin D Affects the Retinal Pigment Epithelium, Impairs Swim-Bladder Ontogenesis and Causes Premature Death in Zebrafish
The lysosomal aspartic protease Cathepsin D (CD) is ubiquitously expressed in eukaryotic organisms. CD activity is essential to accomplish the acid-dependent extensive or partial proteolysis of protein substrates within endosomal and lysosomal compartments therein delivered via endocytosis, phagocytosis or autophagocytosis. CD may also act at physiological pH on small-size substrates in the cytosol and in the extracellular milieu. Mouse and fruit fly CD knock-out models have highlighted the multi-pathophysiological roles of CD in tissue homeostasis and organ development. Here we report the first phenotypic description of the lack of CD expression during zebrafish (Danio rerio) development obtained by morpholino-mediated knock-down of CD mRNA. Since the un-fertilized eggs were shown to be supplied with maternal CD mRNA, only a morpholino targeting a sequence containing the starting ATG codon was effective. The main phenotypic alterations produced by CD knock-down in zebrafish were: 1. abnormal development of the eye and of retinal pigment epithelium; 2. absence of the swim-bladder; 3. skin hyper-pigmentation; 4. reduced growth and premature death. Rescue experiments confirmed the involvement of CD in the developmental processes leading to these phenotypic alterations. Our findings add to the list of CD functions in organ development and patho-physiology in vertebrates
Activation of N-heterocyclic carbenes by {BeH<sub>2</sub>} and {Be(H)(Me)} fragments
A stable three-coordinate dimethylberyllium
species coordinated
by the 1,3-bisÂ(2,4,6-trimethylphenyl)Âimidazol-2-ylidene (IMes) ligand
is readily converted to the corresponding methylhydrido derivative
through metathetical reaction with phenylsilane. Attempts to synthesize
the corresponding molecular dihydrides are, however, unsuccessful
and result in ring opening of an IMes ligand through hydride transfer
to the donor carbon atom and the consequent formation of a heterocyclic
beryllium organoamide. In agreement with previous calculations, we
suggest that this process occurs via a Schlenk-type equilibration
process and formation of a four-coordinate bis-NHC beryllium dihydride.
These species are not observed, however, as the steric pressure exerted
by coordination of the two sterically demanding IMes ligands is sufficient
to induce hydride transfer. The latter deduction is supported by the
observation that a similar ring-opened product, but derived from methyl
and hydride transfer, is available through the introduction of a further
equivalent of IMes to the isolated beryllium methyl hydride species.
In the latter case the ring-opening process is more facile, which
we ascribe to the increased steric pressure achieved upon the formation
of four-coordinate beryllium. In a further striking reaction under
more forcing thermal conditions, the carbene carbon center of an IMes
ligand is observed to be completely eliminated with selective formation
of a three-coordinate diamidoberyllium species
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