@article{IgualGilJariusvonKriesetal.2017,
  author    = {Igual Gil, Carla and Jarius, Mirko and von Kries, Jens P. and Rohlfing, Anne-Kartin},
  title     = {Neuronal Chemosensation and Osmotic Stress Response Converge in the Regulation of aqp-8 in C. elegans},
  series = {Frontiers in physiology},
  volume    = {8},
  journal   = {Frontiers in physiology},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1664-042X},
  doi       = {10.3389/fphys.2017.00380},
  pages     = {12},
  year      = {2017},
  abstract  = {Aquaporins occupy an essential role in sustaining the salt/water balance in various cells types and tissues. Here, we present new insights into aqp-8 expression and regulation in Caenorhabditis elegans. We show, that upon exposure to osmotic stress, aqp-8 exhibits a distinct expression pattern within the excretory cell compared to other C. elegans aquaporins expressed. This expression is correlated to the osmolarity of the surrounding medium and can be activated physiologically by osmotic stress or genetically in mutants with constitutively active osmotic stress response. In addition, we found aqp-8 expression to be constitutively active in the TRPV channel mutant osm-9(ok1677). In a genome-wide RNAi screen we identified additional regulators of aqp-8. Many of these regulators are connected to chemosensation by the amphid neurons, e.g., odr-10 and gpa-6, and act as suppressors of aqp-8 expression. We postulate from our results, that aqp-8 plays an important role in sustaining the salt/water balance during a secondary response to hyper-osmotic stress. Upon its activation aqp-8 promotes vesicle docking to the lumen of the excretory cell and thereby enhances the ability to secrete water and transport osmotic active substances or waste products caused by protein damage. In summary, aqp-8 expression and function is tightly regulated by a network consisting of the osmotic stress response, neuronal chemosensation as well as the response to protein damage. These new insights in maintaining the salt/water balance in C. elegans will help to reveal the complex homeostasis network preserved throughout species.},
  language  = {en}
}
@article{SadowskaKamedaKrupkovaetal.2018,
  author    = {Sadowska, Aleksandra and Kameda, Takuya and Krupkova, Olga and Wuertz-Kozak, Karin},
  title     = {Osmosensing, osmosignalling and inflammation},
  series = {European cells \& materials},
  volume    = {36},
  journal   = {European cells \& materials},
  publisher = {Ao research institute davos-Ari},
  address   = {Davos},
  issn      = {1473-2262},
  doi       = {10.22203/eCM.v036a17},
  pages     = {231 -- 250},
  year      = {2018},
  abstract  = {Intervertebral disc (IVD) cells are naturally exposed to high osmolarity and complex mechanical loading, which drive microenvironmental osmotic changes. Age- and degeneration-induced degradation of the IVD's extracellular matrix causes osmotic imbalance, which, together with an altered function of cellular receptors and signalling pathways, instigates local osmotic stress. Cellular responses to osmotic stress include osmoadaptation and activation of pro-inflammatory pathways. This review summarises the current knowledge on how IVD cells sense local osmotic changes and translate these signals into physiological or pathophysiological responses, with a focus on inflammation. Furthermore, it discusses the expression and function of putative membrane osmosensors (e.g. solute carrier transporters, transient receptor potential channels, aquaporins and acid-sensing ion channels) and osmosignalling mediators [e.g. tonicity response-element-binding protein/nuclear factor of activated T-cells 5 (TonEBP/NFAT5), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)] in healthy and degenerated IVDs. Finally, an overview of the potential therapeutic targets for modifying osmosensing and osmosignalling in degenerated IVDs is provided.},
  language  = {en}
}