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  - 
TY  - GEN
A1  - Sadowska, Aleksandra
A1  - Kameda, Takuya
A1  - Krupkova, Olga
A1  - Würtz-Kozak, Karin
T1  - Osmosensing, osmosignalling and inflammation
BT  - how intervertebral disc cells respond to altered osmolarity
T2  - Postprints der Universität Potsdam : Humanwissenschaftliche Reihe
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 responseelement-binding protein/nuclear factor of activated T-cells 5 (TonEBP/NFAT5), nuclear factor kappa-lightchain-enhancer of activated B cells (NF-kappa B)] in healthy and degenerated IVDs. Finally, an overview of the potential therapeutic targets for modifying osmosensing and osmosignalling in degenerated IVDs is provided.
T3  - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe - 693 
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  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-469080
SN  - 1866-8364
IS  - 693
ER  -