Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.21/2617
Título: Cell-specific regulation of acetylcholinesterase expression under inflammatory conditions
Autor: Oliveira, P. de
Gomes, Anita Q.
Pacheco, T. R.
Vitorino de Almeida, V.
Saldanha, C.
Calado, A.
Palavras-chave: Acetylcholinesterase
Gene expression
Data: Jan-2012
Editora: IOS Press
Citação: Oliveira P, Gomes AQ, Pacheco TR, Vitorino de Almeida V, Saldanha C, Calado A. Cell-specific regulation of acetylcholinesterase expression under inflammatory conditions. 2012;51(2):129-37.
Resumo: Acetylcholine (ACh) has been shown to exert an anti-inflammatory function by down-modulating the expression of pro-inflammatory cytokines. Its availability can be regulated at different levels, namely at its synthesis and degradation steps. Accordingly, the expression of acetylcholinesterase (AChE), the enzyme responsible for ACh hydrolysis, has been observed to be modulated in inflammation. To further address the mechanisms underlying this effect, we aimed here at characterizing AChE expression in distinct cellular types pivotal to the inflammatory response. This study was performed in the human acute leukaemia monocytyc cell line, THP-1, in human monocyte-derived primary macrophages and in human umbilical cord vein endothelial cells (HUVEC). In order to subject these cells to inflammatory conditions, THP-1 and macrophage were treated with lipopolysaccharide (LPS) from E.coli and HUVEC were stimulated with the tumour necrosis factor α (TNF-α). Our results showed that although AChE expression was generally up-regulated at the mRNA level under inflammatory conditions, distinct AChE protein expression profiles were aurprisingly observed among the distinct cellular types studied. Altogether, these results argue for the existence of cell specific mechanisms that regulate the expression of acetylcholinesterase in inflammation.
Peer review: yes
URI: http://hdl.handle.net/10400.21/2617
ISSN: 1875-8622
Versão do Editor: http://iospress.metapress.com/content/6203r303n18k4330/?genre=article&issn=1386-0291&volume=51&issue=2&spage=129
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