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• W2510100774 endingPage "2180" @default.
• W2510100774 startingPage "2166" @default.
• W2510100774 abstract "Multiple sclerosis is a chronic inflammatory, demyelinating degenerative disease of the central nervous system. Current treatments target pathological immune responses to counteract the inflammatory processes. However, these drugs do not restrain the long-term progression of clinical disability. For this reason, new therapeutic approaches and identification of novel target molecules are needed to prevent demyelination or promote repair mechanisms. Transient Receptor Potential Ankyrin 1 (TRPA1) is a nonselective cation channel with relatively high Ca2+ permeability. Its pathophysiological role in central nervous system disorders has not been elucidated yet. In the present study, we aimed to assess the distribution of TRPA1 in the mouse brain and reveal its regulatory role in the cuprizone-induced demyelination. This toxin-induced model, characterized by oligodendrocyte apoptosis and subsequent primary demyelination, allows us to investigate the nonimmune aspects of multiple sclerosis. We found that TRPA1 is expressed on astrocytes in the mouse central nervous system. Interestingly, TRPA1 deficiency significantly attenuated cuprizone-induced demyelination by reducing the apoptosis of mature oligodendrocytes. Our data suggest that TRPA1 regulates mitogen-activated protein kinase pathways, as well as transcription factor c-Jun and a proapoptotic Bcl-2 family member (Bak) expression resulting in enhanced oligodendrocyte apoptosis. In conclusion, we propose that TRPA1 receptors enhancing the intracellular Ca2+ concentration modulate astrocyte functions, and influence the pro or anti-apoptotic pathways in oligodendrocytes. Inhibition of TRPA1 receptors might successfully diminish the degenerative pathology in multiple sclerosis and could be a promising therapeutic target to limit central nervous system damage in demyelinating diseases. GLIA 2016;64:2166–2180" @default.
• W2510100774 created "2016-09-16" @default.
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• W2510100774 date "2016-08-29" @default.
• W2510100774 modified "2023-10-17" @default.
• W2510100774 title "TRPA1 deficiency is protective in cuprizone-induced demyelination-A new target against oligodendrocyte apoptosis" @default.
• W2510100774 cites W1485008662 @default.
• W2510100774 cites W1536622417 @default.
• W2510100774 cites W1554466439 @default.
• W2510100774 cites W1560820741 @default.
• W2510100774 cites W1594876747 @default.
• W2510100774 cites W1790384858 @default.
• W2510100774 cites W181250980 @default.
• W2510100774 cites W1913661233 @default.
• W2510100774 cites W1916136545 @default.
• W2510100774 cites W1967028809 @default.
• W2510100774 cites W1975802844 @default.
• W2510100774 cites W1976385326 @default.
• W2510100774 cites W1977658059 @default.
• W2510100774 cites W1979044083 @default.
• W2510100774 cites W1980249948 @default.
• W2510100774 cites W1980798939 @default.
• W2510100774 cites W1984547206 @default.
• W2510100774 cites W1984636849 @default.
• W2510100774 cites W1987057401 @default.
• W2510100774 cites W1990408451 @default.
• W2510100774 cites W1991883207 @default.
• W2510100774 cites W1996405087 @default.
• W2510100774 cites W1998057701 @default.
• W2510100774 cites W2004715206 @default.
• W2510100774 cites W2007438030 @default.
• W2510100774 cites W2009967312 @default.
• W2510100774 cites W2010795846 @default.
• W2510100774 cites W2011557383 @default.
• W2510100774 cites W2018745308 @default.
• W2510100774 cites W2021786345 @default.
• W2510100774 cites W2026873116 @default.
• W2510100774 cites W2030496214 @default.
• W2510100774 cites W2032911221 @default.
• W2510100774 cites W2040599377 @default.
• W2510100774 cites W2042208155 @default.
• W2510100774 cites W2042528531 @default.
• W2510100774 cites W2047850628 @default.
• W2510100774 cites W2048830609 @default.
• W2510100774 cites W2051385458 @default.
• W2510100774 cites W2053383237 @default.
• W2510100774 cites W2055693317 @default.
• W2510100774 cites W2058117840 @default.
• W2510100774 cites W2058785790 @default.
• W2510100774 cites W2062959517 @default.
• W2510100774 cites W2062993520 @default.
• W2510100774 cites W2069482416 @default.
• W2510100774 cites W2070497927 @default.
• W2510100774 cites W2071946866 @default.
• W2510100774 cites W2072718666 @default.
• W2510100774 cites W2075100277 @default.
• W2510100774 cites W2075819003 @default.
• W2510100774 cites W2076275302 @default.
• W2510100774 cites W2087004322 @default.
• W2510100774 cites W2089154573 @default.
• W2510100774 cites W2089739828 @default.
• W2510100774 cites W2092571234 @default.
• W2510100774 cites W2098719212 @default.
• W2510100774 cites W2109879418 @default.
• W2510100774 cites W2111211230 @default.
• W2510100774 cites W2113679292 @default.
• W2510100774 cites W2113684190 @default.
• W2510100774 cites W2116653422 @default.
• W2510100774 cites W2120229762 @default.
• W2510100774 cites W2122526508 @default.
• W2510100774 cites W2129326126 @default.
• W2510100774 cites W2130292538 @default.
• W2510100774 cites W2133732186 @default.
• W2510100774 cites W2136417207 @default.
• W2510100774 cites W2138246312 @default.
• W2510100774 cites W2139488506 @default.
• W2510100774 cites W2147062889 @default.
• W2510100774 cites W2147503051 @default.
• W2510100774 cites W2152247516 @default.
• W2510100774 cites W2156549416 @default.
• W2510100774 cites W2160412284 @default.
• W2510100774 cites W2164837602 @default.
• W2510100774 cites W2168073506 @default.
• W2510100774 cites W2238771054 @default.
• W2510100774 cites W2265455913 @default.
• W2510100774 cites W2332618518 @default.
• W2510100774 cites W256530927 @default.
• W2510100774 cites W262445822 @default.

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