Matches in SemOpenAlex for { <https://semopenalex.org/work/W3137163905> ?p ?o ?g. }
- W3137163905 endingPage "1708" @default.
- W3137163905 startingPage "1694" @default.
- W3137163905 abstract "Microglia are intrinsic immune cells that release factors including pro- and anti-inflammatory cytokines, nitric oxide (NO) and neurotrophins following activation in the brain. Elevation of intracellular Ca2+ concentration ([Ca2+ ]i) is important for microglial functions, such as the release of cytokines or NO from activated microglia. Brain-derived neurotrophic factor (BDNF) is a neurotrophin well known for its roles in the activation of microglia. Interestingly, proBDNF, the precursor form of mature BDNF, and mature BDNF elicit opposing neuronal responses in the brain. Mature BDNF induces sustained intracellular Ca2+ elevation through the upregulation of the surface expression of TRPC3 channels in rodent microglial cells. In addition, TRPC3 channels are important for the BDNF-induced suppression of NO production in activated microglia. In this study, we observed that proBDNF and mature BDNF have opposite effects on the relative expression of surface p75 neurotrophin receptor (p75NTR ) in rodent microglial cells. ProBDNF induces a sustained elevation of [Ca2+ ]i through binding to the p75NTR , which is possibly mediated by Rac 1 activation and TRPM7 channels in rodent microglial cells. Flow cytometry showed that proBDNF increased the relative surface expression of TRPM7. Although proBDNF did not affect either mRNA expression of pro- and anti-inflammatory cytokines or the phagocytic activity, proBDNF potentiates the generation of NO induced by IFN-γ and TRPM7 channels could be involved in the proBDNF-induced potentiation of IFN-γ-mediated production of NO. We show direct evidence that rodent microglial cells are able to respond to proBDNF, which might be important for the regulation of inflammatory responses in the brain." @default.
- W3137163905 created "2021-03-29" @default.
- W3137163905 creator A5011048360 @default.
- W3137163905 creator A5012151901 @default.
- W3137163905 creator A5035087249 @default.
- W3137163905 creator A5052182246 @default.
- W3137163905 creator A5069412415 @default.
- W3137163905 creator A5080408080 @default.
- W3137163905 date "2021-03-19" @default.
- W3137163905 modified "2023-09-23" @default.
- W3137163905 title "<scp>ProBDNF</scp> induces sustained elevation of intracellular Ca <sup>2+</sup> possibly mediated by <scp>TRPM7</scp> channels in rodent microglial cells" @default.
- W3137163905 cites W1489975469 @default.
- W3137163905 cites W1513750861 @default.
- W3137163905 cites W1519576356 @default.
- W3137163905 cites W1553814286 @default.
- W3137163905 cites W1558107540 @default.
- W3137163905 cites W1600123087 @default.
- W3137163905 cites W1692776653 @default.
- W3137163905 cites W1813872274 @default.
- W3137163905 cites W1851114555 @default.
- W3137163905 cites W1914637174 @default.
- W3137163905 cites W1921896771 @default.
- W3137163905 cites W1965909642 @default.
- W3137163905 cites W1967347247 @default.
- W3137163905 cites W1970899777 @default.
- W3137163905 cites W1973854181 @default.
- W3137163905 cites W1981764021 @default.
- W3137163905 cites W1982504898 @default.
- W3137163905 cites W1982788061 @default.
- W3137163905 cites W2003066006 @default.
- W3137163905 cites W2004107819 @default.
- W3137163905 cites W2010055809 @default.
- W3137163905 cites W2017167787 @default.
- W3137163905 cites W2017549750 @default.
- W3137163905 cites W2023709895 @default.
- W3137163905 cites W2027018469 @default.
- W3137163905 cites W2030448361 @default.
- W3137163905 cites W2031141543 @default.
- W3137163905 cites W2033045687 @default.
- W3137163905 cites W2033608496 @default.
- W3137163905 cites W2035936653 @default.
- W3137163905 cites W2045019886 @default.
- W3137163905 cites W2046608695 @default.
- W3137163905 cites W2050808516 @default.
- W3137163905 cites W2052152153 @default.
- W3137163905 cites W2063535351 @default.
- W3137163905 cites W2064816991 @default.
- W3137163905 cites W2066386560 @default.
- W3137163905 cites W2067040581 @default.
- W3137163905 cites W2067267561 @default.
- W3137163905 cites W2067302534 @default.
- W3137163905 cites W2083817323 @default.
- W3137163905 cites W2084861108 @default.
- W3137163905 cites W2085487753 @default.
- W3137163905 cites W2087244638 @default.
- W3137163905 cites W2090693552 @default.
- W3137163905 cites W2096500024 @default.
- W3137163905 cites W2100433008 @default.
- W3137163905 cites W2107831782 @default.
- W3137163905 cites W2109309568 @default.
- W3137163905 cites W2122071004 @default.
- W3137163905 cites W2124836944 @default.
- W3137163905 cites W2127548642 @default.
- W3137163905 cites W2128294582 @default.
- W3137163905 cites W2128994172 @default.
- W3137163905 cites W2137258759 @default.
- W3137163905 cites W2143210066 @default.
- W3137163905 cites W2143782901 @default.
- W3137163905 cites W2158861376 @default.
- W3137163905 cites W2170158378 @default.
- W3137163905 cites W2170490236 @default.
- W3137163905 cites W2208257007 @default.
- W3137163905 cites W2292155060 @default.
- W3137163905 cites W2423884004 @default.
- W3137163905 cites W2497241389 @default.
- W3137163905 cites W2508885228 @default.
- W3137163905 cites W2591587397 @default.
- W3137163905 cites W2614127212 @default.
- W3137163905 cites W2617437623 @default.
- W3137163905 cites W2619332462 @default.
- W3137163905 cites W2779644013 @default.
- W3137163905 cites W2795628695 @default.
- W3137163905 cites W2883313035 @default.
- W3137163905 cites W2895880152 @default.
- W3137163905 cites W2902557925 @default.
- W3137163905 cites W2907357165 @default.
- W3137163905 cites W2922810409 @default.
- W3137163905 cites W2939978680 @default.
- W3137163905 cites W2971923367 @default.
- W3137163905 cites W2980347030 @default.
- W3137163905 cites W2991312362 @default.
- W3137163905 cites W3089473754 @default.
- W3137163905 cites W4240168071 @default.
- W3137163905 cites W4253096340 @default.
- W3137163905 doi "https://doi.org/10.1002/glia.23996" @default.
- W3137163905 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33740269" @default.
- W3137163905 hasPublicationYear "2021" @default.
- W3137163905 type Work @default.