@article{BrieseSaalAppenzelleretal.2015,
  author    = {Briese, Michael and Saal, Lena and Appenzeller, Silke and Moradi, Mehri and Baluapuri, Apoorva and Sendtner, Michael},
  title     = {Whole transcriptome profiling reveals the RNA content of motor axons},
  series = {Nucleic Acids Research},
  journal   = {Nucleic Acids Research},
  doi       = {10.1093/nar/gkv1027},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126800},
  year      = {2015},
  abstract  = {Most RNAs within polarized cells such as neurons are sorted subcellularly in a coordinated manner. Despite advances in the development of methods for profiling polyadenylated RNAs from small amounts of input RNA, techniques for profiling coding and non-coding RNAs simultaneously are not well established. Here, we optimized a transcriptome profiling method based on double-random priming and applied it to serially diluted total RNA down to 10 pg. Read counts of expressed genes were robustly correlated between replicates, indicating that the method is both reproducible and scalable. Our transcriptome profiling method detected both coding and long non-coding RNAs sized >300 bases. Compared to total RNAseq using a conventional approach our protocol detected 70\% more genes due to reduced capture of ribosomal RNAs. We used our method to analyze the RNA composition of compartmentalized motoneurons. The somatodendritic compartment was enriched for transcripts with post-synaptic functions as well as for certain nuclear non-coding RNAs such as 7SK. In axons, transcripts related to translation were enriched including the cytoplasmic non-coding RNA 7SL. Our profiling method can be applied to a wide range of investigations including perturbations of subcellular transcriptomes in neurodegenerative diseases and investigations of microdissected tissue samples such as anatomically defined fiber tracts.},
  language  = {en}
}
@article{SimonRauskolbGunnersenetal.2015,
  author    = {Simon, Christian M. and Rauskolb, Stefanie and Gunnersen, Jennifer M. and Holtmann, Bettina and Drepper, Carsten and Dombert, Benjamin and Braga, Massimiliano and Wiese, Stefan and Jablonka, Sibylle and P{\"u}hringer, Dirk and Zielasek, J{\"u}rgen and Hoeflich, Andreas and Silani, Vincenzo and Wolf, Eckhard and Kneitz, Susanne and Sommer, Claudia and Toyka, Klaus V. and Sendtner, Michael},
  title     = {Dysregulated IGFBP5 expression causes axon degeneration and motoneuron loss in diabetic neuropathy},
  series = {Acta Neuropathologica},
  volume    = {130},
  journal   = {Acta Neuropathologica},
  doi       = {10.1007/s00401-015-1446-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-154569},
  pages     = {373 -- 387},
  year      = {2015},
  abstract  = {Diabetic neuropathy (DNP), afflicting sensory and motor nerve fibers, is a major complication in diabetes.The underlying cellular mechanisms of axon degeneration are poorly understood. IGFBP5, an inhibitory binding protein for insulin-like growth factor 1 (IGF1) is highly up-regulated in nerve biopsies of patients with DNP. We investigated the pathogenic relevance of this finding in transgenic mice overexpressing IGFBP5 in motor axons and sensory nerve fibers. These mice develop motor axonopathy and sensory deficits similar to those seen in DNP. Motor axon degeneration was also observed in mice in which the IGF1 receptor(IGF1R) was conditionally depleted in motoneurons, indicating that reduced activity of IGF1 on IGF1R in motoneurons is responsible for the observed effect. These data provide evidence that elevated expression of IGFBP5 in diabetic nerves reduces the availability of IGF1 for IGF1R on motor axons, thus leading to progressive neurodegeneration. Inhibition of IGFBP5 could thus offer novel treatment strategies for DNP.},
  language  = {en}
}