It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Nociceptors are a particular subtype of dorsal root ganglion (DRG) neurons that detect noxious stimuli and elicit pain. Although recent efforts have been made to reveal the molecular profile of nociceptors in normal conditions, little is known about how this profile changes in pathological conditions. In this study we exploited laser capture microdissection to specifically collect individual injured and non-injured nociceptive DRG neurons and to define their gene profiling in rat spared nerve injury (SNI) model of neuropathic pain. We found minimal transcriptional changes in non-injured neurons at 7 days after SNI. In contrast, several novel transcripts were altered in injured nociceptors, and the global signature of these LCM-captured neurons differed markedly from that the gene expression patterns found previously using whole DRG tissue following SNI. Pathway analysis of the transcriptomic profile of the injured nociceptors revealed oxidative stress as a key biological process. We validated the increase of caspase-6 (CASP6) in small-sized DRG neurons and its functional role in SNI- and paclitaxel-induced neuropathic pain. Our results demonstrate that the identification of gene regulation in a specific population of DRG neurons (e.g., nociceptors) is an effective strategy to reveal new mechanisms and therapeutic targets for neuropathic pain from different origins.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Pain Center, Department of anesthesiology, Lausanne University Hospital (CHUV) and Faculty of biology and medicine (FBM), University of Lausanne (UNIL), Lausanne, Switzerland; Department of Anesthesiology, Duke University Medical Center, 595 LaSalle Street, Durham, NC, USA; Pain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, Ohio, USA
2 Department of Basic Neuroscience, Faculty of Medicine, Geneva, Switzerland; University of Montpellier, Montpellier, F-34095 France, INSERM, U1198, Montpellier, F-34095 France, EPHE, Paris, France
3 Pain Center, Department of anesthesiology, Lausanne University Hospital (CHUV) and Faculty of biology and medicine (FBM), University of Lausanne (UNIL), Lausanne, Switzerland; Department of Fundamental Neurosciences, Faculty of biology and medicine (FBM), University of Lausanne (UNIL), Lausanne, Switzerland
4 Pain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, Ohio, USA
5 Department of Anesthesiology, College of Medicine, National Cheng Kung University, Tainan city, Taiwan
6 Department of Anesthesiology, Duke University Medical Center, 595 LaSalle Street, Durham, NC, USA
7 Department of Basic Neuroscience, Faculty of Medicine, Geneva, Switzerland