TY - JOUR A1 - Igual Gil, Carla A1 - Jarius, Mirko A1 - von Kries, Jens P. A1 - Rohlfing, Anne-Kartin T1 - Neuronal Chemosensation and Osmotic Stress Response Converge in the Regulation of aqp-8 in C. elegans JF - Frontiers in physiology N2 - 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. KW - aquaporin KW - osmoregulation KW - osmotic stress KW - chemosensation KW - C. elegans Y1 - 2017 U6 - https://doi.org/10.3389/fphys.2017.00380 SN - 1664-042X VL - 8 PB - Frontiers Research Foundation CY - Lausanne ER - TY - JOUR A1 - Sadowska, Aleksandra A1 - Kameda, Takuya A1 - Krupkova, Olga A1 - Wuertz-Kozak, Karin T1 - Osmosensing, osmosignalling and inflammation BT - how intervertebral disc cells respond to altered osmolarity JF - European cells & materials N2 - 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. KW - Intervertebral disc degeneration KW - degenerative disc disease KW - osmolarity KW - hyper-osmolarity KW - hypo-osmolarity KW - osmotic KW - inflammatory KW - transient receptor potential channel KW - aquaporin KW - tonicity-responsive enhancer binding protein Y1 - 2018 U6 - https://doi.org/10.22203/eCM.v036a17 SN - 1473-2262 VL - 36 SP - 231 EP - 250 PB - Ao research institute davos-Ari CY - Davos ER -