In JoVE (1)
Articles by Christian Njoo in JoVE
I Vivo siRNA Transfection og Gene Knockdown i Spinal Cord via Rapid Noninvasiv Lumbar Intratekal Injeksjoner i Mus Christian Njoo1, Celine Heinl1, Rohini Kuner1 1Institute for Pharmacology, University of Heidelberg Denne rapporten beskriver en enkel og rask teknikk av intratekal nålestikk for en lokalisert transfeksjon av siRNA i ryggmargen i mus på korte varig lett anestesi.
Other articles by Christian Njoo on PubMed
Hematopoietic Colony-stimulating Factors Mediate Tumor-nerve Interactions and Bone Cancer Pain Nature Medicine. Jul, 2009 | Pubmed ID: 19525966 Pain is one of the most severe and debilitating symptoms associated with several forms of cancer. Various types of carcinomas and sarcomas metastasize to skeletal bones and cause spontaneous bone pain and hyperalgesia, which is accompanied by bone degradation and remodeling of peripheral nerves. Despite recent advances, the molecular mechanisms underlying the development and maintenance of cancer-evoked pain are not well understood. Several types of non-hematopoietic tumors secrete hematopoietic colony-stimulating factors that act on myeloid cells and tumor cells. Here we report that receptors and signaling mediators of granulocyte- and granulocyte-macrophage colony-stimulating factors (G-CSF and GM-CSF) are also functionally expressed on sensory nerves. GM-CSF sensitized nerves to mechanical stimuli in vitro and in vivo, potentiated CGRP release and caused sprouting of sensory nerve endings in the skin. Interruption of G-CSF and GM-CSF signaling in vivo led to reduced tumor growth and nerve remodeling, and abrogated bone cancer pain. The key significance of GM-CSF signaling in sensory neurons was revealed by an attenuation of tumor-evoked pain following a sensory nerve-specific knockdown of GM-CSF receptors. These results show that G-CSF and GM-CSF are important in tumor-nerve interactions and suggest that their receptors on primary afferent nerve fibers constitute potential therapeutic targets in cancer pain.
A Novel Biological Role for the Phospholipid Lysophosphatidylinositol in Nociceptive Sensitization Via Activation of Diverse G-protein Signalling Pathways in Sensory Nerves in Vivo Pain. Dec, 2013 | Pubmed ID: 23973358 The rich diversity of lipids and the specific signalling pathways they recruit provides tremendous scope for modulation of biological functions. Lysophosphatidylinositol (LPI) is emerging as a key modulator of cell proliferation, migration, and function, and holds important pathophysiological implications due to its high levels in diseased tissues, such as in cancer. Here we report a novel role for LPI in sensitization of peripheral sensory neurons, which was evident as exaggerated sensitivity to painful and innocuous pressure. Histopathological analyses indicated lack of involvement of myelin pathology and immune cell recruitment by LPI. Using pharmacological and conditional genetic tools in mice, we delineated receptor-mediated from non-receptor-mediated effects of LPI and we observed that GPR55, which functions as an LPI receptor when heterologously expressed in mammalian cells, only partially mediates LPI-induced actions in the context of pain sensitization in vivo; we demonstrate that, in vivo, LPI functions by activating Gα(13) as well as Gα(q/11) arms of G-protein signalling in sensory neurons. This study thus reports a novel pathophysiological function for LPI and elucidates underlying molecular mechanisms.