Modulation in the expression of SHP-1, SHP-2 and PTP1B due to the inhibition of MAPKs, cAMP and neutrophils early on in the development of cerulein-induced acute pancreatitis in rats

[EN]The protein tyrosine phosphatases (PTPs) SHP-1, SHP-2 and PTP1B are overexpressed early on during the development of cerulein -induced acute pancreatitis (AP) in rats, and their levels can be modulated by some species of mitogen-activated protein kinases (MAPKs), the intracellular levels of cAMP...

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Detalles Bibliográficos
Autores: García Hernández, Violeta, Sarmiento, Nancy, Sánchez Bernal, María Carmen, Pascual Matellán, Laura, Calvo Andrés, José Julián, Sánchez Yagüe, Jesús
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2014
País:España
Institución:Universidad de Salamanca (USAL)
Repositorio:GREDOS. Repositorio Institucional de la Universidad de Salamanca
OAI Identifier:oai:gredos.usal.es:10366/155156
Acceso en línea:http://hdl.handle.net/10366/155156
Access Level:acceso embargado
Palabra clave:Experimental acute pancreatitis
SHP-1
SHP-2
PTP1B
MAPK inhibition
Infiltration inhibition
Anthracenes
Acute Disease
Flavonoids
Immunoblotting
Ceruletide
Neutrophil Infiltration
Cyclic AMP
Pancreas
Mitogen-Activated Protein Kinases
Time Factors
Rats
Immunohistochemistry
Animals
JNK Mitogen-Activated Protein Kinases
Mitogen-Activated Protein Kinase 3
Pancreatitis
Mitogen-Activated Protein Kinase 1
inmunohistoquímica
factores de tiempo
pancreatitis
proteína cinasa activada por mitógenos 1
proteína cinasas activadas por mitógenos
ceruletida
inmunotransferencia
enfermedad aguda
flavonoides
proteína cinasa activada por mitógenos 3
animales
infiltración de neutrófilos
antracenos
proteína cinasas JNK activadas por mitógenos
ratas
AMP cíclico
páncreas
Descripción
Sumario:[EN]The protein tyrosine phosphatases (PTPs) SHP-1, SHP-2 and PTP1B are overexpressed early on during the development of cerulein -induced acute pancreatitis (AP) in rats, and their levels can be modulated by some species of mitogen-activated protein kinases (MAPKs), the intracellular levels of cAMP and by general leukocyte infiltration, the latter at least for SHP-2 and PTP1B. In this study we show that cerulein treatment activates extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) but not p38 MAPK during the early phase of cerulein-induced AP (2h after the first injection of cerulein). Therefore, by using the MAPK inhibitors SP600125 (a specific JNK inhibitor) and PD98059 (a specific ERK inhibitor), we have unmasked the particular MAPK that underlies the modulation of the expression levels of these PTPs. JNK would act by preventing SHP-1 protein expression from increasing beyond a certain level. ERK 1/2 was the main MAPK involved in the increase in SHP-2 protein expression due to cerulein. JNK negatively modulated the SH2-domain containing PTPs. Both MAPKs played a role in the increase in PTP1B protein expression due to cerulein. Finally, by using the white blood cell inhibitors vinblastine sulfate, gadolinium chloride and FK506 (tacrolimus), we show that the macrophage activity or T-lymphocytes does not modulate the expression of any of the PTPs, although neutrophil infiltration was found to be a regulator of SHP-2 and PTP1B protein expression due to cerulein.