Acute-phase response of the rat pancreas protects against further aggression with severe necrotizing pancreatitis

Fiedler, Fritz; Croissant, N; Rehbein, C; Iovanna, Juan; Dagorn, Jean–Charles; Ackern, K. van; Keim, Volker

doi:10.1097/00003246-199805000-00024

Cited by 32 publications

(9 citation statements)

References 32 publications

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“…), it was speculated that PAP could act as a cell response to the inflammatory stress. This is in line with the fact that induction in the pancreas of an acute-phase response, in which PAP expression was activated, prior to triggering necrotizing pancreatitis, significantly improved the survival of the animals [36] . Studies demonstrated that the administration of anti-PAP antibodies in an experimental model of taurocholate-induced acute pancreatitis in rats was associated with increased inflammation in the pancreas, evidenced by more abundant necrosis, increased pancreatic myeloperoxidase (MPO) levels and more prominent neutrophil infiltration [37] .…”

Section: Pap As An Anti-inflammatory Mediatorsupporting

confidence: 78%

Pancreatitis-associated protein: From a lectin to an anti-inflammatory cytokine

Closa

Motoo²,

Iovanna³

2007

WJG

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Pancreatitis-associated protein (PAP) was discovered in the pancreatic juice of rats with acute pancreatitis. PAP is a 16 kDa secretory protein structurally related to the C-type lectins although classical lectin-related function has not been reported yet. Then, it was demonstrated that PAP expression may be activated in some tissues in a constitutive or injury-and inflammation-induced manner. More recently, it has been found that PAP acts as an anti-inflammatory factor in vitro and in vivo .PAP expression can be induced by several pro-and anti-inflammatory cytokines and by itself through a JAK/STAT3-dependent pathway. PAP is able to activate the expression of the anti-inflammatory factor SOCS3 through the JAK/STAT3-dependent pathway. The JAK/STAT3/SOCS3 pathway seems to be a common point between PAP and several cytokines. Therefore, it is reasonable to propose that PAP is a new antiinflammatory cytokine.

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Section: Pap As An Anti-inflammatory Mediatorsupporting

confidence: 78%

Pancreatitis-associated protein: From a lectin to an anti-inflammatory cytokine

Closa

Motoo²,

Iovanna³

2007

WJG

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“…Expression of the antiproliferation gene encoding TIS21 is induced upon DNA damage in cell lines, while cells with a targeted disruption in the TIS21 gene fail to undergo cell cycle arrest in response to DNA damage (48). In addition, TIS21 expression is induced in kidney and liver during acute pancreatitis and is thought to play a role in the control of apoptosis progression in these tissues (11).…”

Section: Resultsmentioning

confidence: 99%

Pro-B-Cell-Specific Transcription and Proapoptotic Function of Protein Kinase Cη

Morrow

Muljo

Zhang

et al. 1999

Molecular and Cellular Biology

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Using a subtractive cloning scheme on cDNA prepared from primary pro-B and pre-B cells, we identified several genes whose products regulate apoptosis. We further characterized one of these genes, encoding protein kinase C (PKC). PKC transcripts were readily detected in pro-B cells but were absent in pre-B cells. Although both a full-length and a truncated form of PKC were detectable in bone marrow pro-B cells, transition to the pre-B-cell stage was associated with increased relative levels of truncated PKC. We found that PKC is proteolyzed in apoptotic lymphocytes, generating a kinase-active fragment identical to the truncated form which is capable of inducing apoptosis when expressed in a pro-B cell line. Caspase-3 can generate an identical PKC cleavage product in vitro, and caspase inhibitors prevent the generation of this product during apoptosis in transfected cell lines. Inducible overexpression of either the full-length or truncated form of PKC results in cell cycle arrest at the G 1 /S transition. These results suggest that the expression and proteolytic activation of PKC play an important role in the regulation of cell division and cell death during early B-cell development.

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“…REG3A is indeed an acute phase protein with an exocrine nature, whose synthesis and processing follows the acinar cell secretory pathway, from the endoplasmic reticulum to the zymogen granules [29,30]. REG3A was shown to act as a protective factor against pancreas damage [19,31,32]. It is therefore remarkable that the rise in the concentration of secretory pathwayassociated proteins observed by proteomic analysis and immunoassays coincided with the burst of REG3A expression.…”

Section: Discussionmentioning

confidence: 95%

Time-course proteomic analysis of taurocholate-induced necrotizing acute pancreatitis

Fétaud-Lapierre

Pastor

Jorge-Costa

et al. 2013

Journal of Proteomics

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Acute pancreatitis is an inflammatory disease of the pancreas, which varies greatly in course and severity. Severe forms are associated with serious local and/or systemic complications, and eventually death. The pathobiology of acute pancreatitis is complex.Animal models have been developed to investigate pathobiological processes and identify factors determining disease course. We performed a time-course proteomic analysis using a rat model of severe necrotizing acute pancreatitis induced by taurocholate perfusion in the pancreatic ducts. Results showed that levels of proteins associated to a given biological process changed in a coordinated fashion after disease onset. It was possible to follow the response of a particular pathobiological process to pancreatitis induction and to compare the course of protein pathways. Proteins involved in acinar cell secretion were found to follow a different kinetics than other cellular processes. After an initial decrease, secretory pathway-associated proteins raised again at 18 h post-induction. This phenomenon coincided with a burst in the expression of pancreatitis-associated protein (REG3A), an acute phase protein produced by the exocrine pancreas, and with the decrease of classical markers of pancreatic injury, suggesting that the expression of proteins associated to the secretory pathway may be a modulating factor of pancreas injury. S 8 5 ( 2 0 1 3 ) 1 2 -2 7Abbreviations: AP, acute pancreatitis; MS, mass spectrometry; MPO, myeloperoxidase; IHC, immunohistochemistry; LACB, bovine ß-lactoglobulin; CV, coefficient of variation; GO, gene ontology; A1I3, alpha-1-inhibitor 3; REG3A, pancreatitis-associated protein 1; GP2, pancreatic secretory granule membrane major glycoprotein; COPD, coatomer delta; COPB, coatomer beta. ☆ This study was supported by grants from the Swiss National Science Foundation no. 320000-120021 and no. 320000-113225/1. by a severe disease with pancreatic necrosis and systemic inflammation. The objectives of this study were to determine the kinetics of functionally related proteins in the early steps of the experimental disease in order to identify protein pathways playing key roles in AP pathobiology and to correlate these data with parameters classically used to assess disease severity. The present work provides for the first time an overview of protein expression in the pancreas during the course of taurocholate-induced necrotizing AP. We believe that correlation of these results with data obtained using proteomic or biochemical approaches in various experimental models of AP will help in highlighting new features, generating hypotheses and constitute therefore a strong and reliable basis for further targeted investigations.

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Acute-phase response of the rat pancreas protects against further aggression with severe necrotizing pancreatitis

Cited by 32 publications

References 32 publications

Pancreatitis-associated protein: From a lectin to an anti-inflammatory cytokine

Pancreatitis-associated protein: From a lectin to an anti-inflammatory cytokine

Pro-B-Cell-Specific Transcription and Proapoptotic Function of Protein Kinase Cη

Time-course proteomic analysis of taurocholate-induced necrotizing acute pancreatitis

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