Changes in the expression of LIMP-2 during cerulein-induced pancreatitis in rats: Effect of inhibition of leukocyte infiltration, cAMP and MAPKs early on in its development
| Autor: | Jesús Sánchez-Yagüe, Carmen Sánchez-Bernal, Angel Hernández-Hernández, Nancy Sarmiento, Violeta García-Hernández, Rafael Coveñas, José Julián Calvo |
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| Rok vydání: | 2016 |
| Předmět: |
CD36 Antigens
Male 0301 basic medicine medicine.medical_specialty Biochemistry 03 medical and health sciences Internal medicine Cyclic AMP medicine Animals Rats Wistar Phosphodiesterase inhibitor Ceruletide Rolipram Kinase Chemistry Lysosome-Associated Membrane Glycoproteins Cell Biology medicine.disease Rats 030104 developmental biology Endocrinology Gene Expression Regulation Neutrophil Infiltration Pancreatitis Acute pancreatitis Mitogen-Activated Protein Kinases Signal transduction Immunostaining Signal Transduction medicine.drug |
| Zdroj: | The International Journal of Biochemistry & Cell Biology. 72:109-117 |
| ISSN: | 1357-2725 |
| DOI: | 10.1016/j.biocel.2016.01.010 |
| Popis: | Lysosomal integral membrane protein-2 (LIMP-2) is an important protein in lysosomal biogenesis and function and also plays a role in the tissue inflammatory response. It is known that lysosomes play a central role in acute pancreatitis, with inflammatory cell infiltration triggering the disease early on. In this study we report increases in pancreatic LIMP-2 protein and mRNA levels as early events that occur during the development of cerulein (Cer)-induced acute pancreatitis (AP) in rats. GdCl3, a macrophage inhibitor, but not FK506, a T lymphocyte inhibitor, was able to reverse the increase in LIMP-2 expression after Cer treatment, although such reversion was abolished if the animals were depleted of neutrophils due to a vinblastine sulfate pre-treatment. Immunostaining revealed that the cellular source of LIMP-2 was mainly acinar cells. Additionally, pre-treatments with the MAPKs inhibitors SP600125 and PD98059, inhibitors of JNK and ERK½ activation, respectively, but not of rolipram, a type IV phosphodiesterase inhibitor, suppressed the increase in the expression of LIMP-2 after Cer administration. Together, these results indicate that neutrophils are able to drive a macrophage activation that would regulate the increase in LIMP-2 expression during the early phase of Cer-induced AP, with the stress kinases JNK and ERK½ also playing a coordinated role in the increase of LIMP-2 expression due to Cer. |
| Databáze: | OpenAIRE |
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