RT info:eu-repo/semantics/article
T1 Signal transduction of MCP-1 expression induced by pancreatitis-associated ascitic fluid in pancreatic acinar cells
A1 Ramudo, Laura
A1 Yubero Benito, Sara
A1 Manso, Manuel Antonio
A1 Vicente, Secundino
A1 Dios, Isabel de
K1 Acinar cells
K1 Células acinares
K1 Dexamethasone
K1 Dexametasona
K1 N-acetylcysteine
K1 N-acetilcisteína
K1 Ascites
K1 Ascitis
AB Pancreatitis-associated ascitic fluid (PAAF) is known to contribute to the progression of acute pancreatitis (AP). We have investigated the capability of PAAF to activate the expression of MCP-1 in pancreatic acinar cells and the involvement of MAPK, NF-κB and STAT3 as downstream signalling transduction pathways. The actions of dexamethasone (Dx) and N-acetylcysteine (NAC) on the PAAF's acinar effects have also been evaluated. Acinar cells were incubated for 1 hr with PAAF collected from rats with severe AP induced by sodium taurocholate in the absence or presence of Dx (10−7 M) or NAC (30 mM). MCP-1 mRNA expression, phospho-p38-MAPK, IκBα, nuclear p65 levels and nuclear translocation of STAT3 were analysed. In response to PAAF, overexpression of MCP-1, phosphorylation of p38-MAPK, degradation of IκBα and increases in p65 nuclear levels and STAT3 activity were found in acinar cells. PAAF-mediated MCP-1 up-regulation was completely suppressed by Dx and NAC. MAPK activation was only inhibited by NAC, NF-κB activation was repressed by Dx and NAC, and STAT3 pathway was strongly blocked by Dx and significantly reduced by NAC. In conclusion, acinar cells were activated by PAAF to produce MCP-1, mainly via NF-κB and STAT3 pathways. Both downstream pathways were targeted by Dx and NAC to repress the PAAF-mediated acinar MCP-1 up-regulation.
PB Wiley
SN 1582-4934
YR 2009
FD 2009
LK https://uvadoc.uva.es/handle/10324/46970
UL https://uvadoc.uva.es/handle/10324/46970
LA eng
NO Journal of Cellular and Molecular Medicine, 2009, vol. 13, n. 7. p. 1314-1320
NO Producción Científica
DS UVaDOC
RD 26-abr-2024