Pancreatic damage induced by injecting a large dose of arginine

Kawaguchi, Yasuo; Kawamura, Sumio

doi:10.1007/bf02890197

Cited by 33 publications

(20 citation statements)

References 10 publications

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“…Partial dilatation or vacuolation of the ER cisternea is the earliest change observed after intraperitoneal injection of arginine -another model of acute pancreatitis [82,83]. Pancreatic duct ligation induced massive dilatation of the rough ER in an opossum model [84]. Changes in pancreatic ER histology have also been noted in samples from human pancreata under shock situations [85].…”

Section: Er Stress Occurs During Acute Pancreatitismentioning

confidence: 95%

Endoplasmic reticulum stress and the pancreatic acinar cell

Kubisch

Logsdon

2008

Expert Review of Gastroenterology & Hepatology

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The pancreas is the primary organ responsible for the digestion of food. Pancreatic acinar cells are specialized for the production of digestive enzymes, and these cells have a higher rate of protein synthesis than all other adult human tissues. Digestive enzymes are produced in the endoplasmic reticulum (ER), a multifunctional organelle responsible for the synthesis and correct folding of proteins in the secretory pathway. Disturbances of ER function lead to stress-response mechanisms that can restore homeostasis but can also, if uncontrolled, cause disease. Pancreatic acinar cells are particularly susceptible to ER perturbations, and mechanisms that relieve ER stress are necessary for normal pancreatic development. Furthermore, ER stress occurs during acute pancreatitis, and may also be present in pancreatic cancer. However, the specific roles of ER stress-response mechanisms in these diseases are unknown.

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Section: Er Stress Occurs During Acute Pancreatitismentioning

confidence: 95%

Endoplasmic reticulum stress and the pancreatic acinar cell

Kubisch

Logsdon

2008

Expert Review of Gastroenterology & Hepatology

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“…WBN/Kob rats [15,23], OLETF rats [4], and Aly mice [14] are known to develop pancreatitis spontaneously, and experimental pancreatitis can be induced by ethanol feeding [24] or arginine injection [6] in rats or mice. These conditions have thus been utilized as models for human pancreatitis.…”

Section: Introductionmentioning

confidence: 99%

Histopathological and biochemical studies on pancreatic fibrosis in WBN/Kob rats

1999

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We investigated the time-course of changes in pancreatic fibrosis accompanied with pancreatitis in WBN/Kob rats. The areas of fibrosis and fatty replacement were analysed morphometrically, and biochemical measurements of pancreatic and plasma prolyl hydroxylase and of pancreatic collagenase were assessed. Male rats showed acute pancreatitis at 2-3 months of age, lesions that later underwent a transition to widespread fibrosis. The fibrosis then decreased, and the fibrotic tissue was replaced with adipose tissue. Morphometrically, the fibrotic area reached its maximal size when the rats were 4 months old, diminishing thereafter. The fibrosis occurred mainly in the intralobular space, and was principally attributable to type-III collagen. Type-I collagen scarcely appeared throughout the experimental period. Alpha-Smooth muscle actin appeared in and around myofibroblasts that developed in an early stage and diminished later in accordance with the progressive manner of fibrosis. The plasma prolyl hydroxylase level was higher in males than in females from 4 through 10 months of age. Pancreatic collagenase activity in the males also increased during the same period. These findings suggest that pancreatic fibrosis in male WBN/Kob rats is affected by the balance between prolyl hydroxylase and collagenase.

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“…17 18 This model is non-invasive and has a defined time course following initiation by a single intraperitoneal injection of arginine. Recently it has been used to investigate regeneration following acute necrotising pancreatitis 19…”

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Arginine induced acute pancreatitis alters the actin cytoskeleton and increases heat shock protein expression in rat pancreatic acinar cells

Tashiro

Schäfer

Yao

et al. 2001

Gut

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Arginine induced acute pancreatitis was evaluated as a novel and distinct form of experimental pancreatitis with particular attention to the actin cytoskeleton and expression of heat shock or stress proteins. Arginine induced a dose related necrotising pancreatitis in rats, as shown by histological evaluation, and an increase in serum amylase. Severe pancreatitis induced by 4.5 g/kg arginine was accompanied by dramatic changes in the actin cytoskeleton, as visualised with rhodamine phallodin. Intermediate filaments were also disrupted, as visualised by cytokeratin 8/18 immunocytochemistry. Arginine pancreatitis was accompanied by a stress response with a large increase in the small heat shock protein HSP27, as well as HSP70, peaking at 24 hours and localised to acinar cells. There was a lower increase in HSP60 and HSP90 and no eVect on GRP78. HSP27 was also shifted to phosphorylated forms during pancreatitis. A lower dose of arginine (3.0 g/kg) induced less pancreatitis but a larger increase in HSP70 and HSP27 expression and phosphorylation of HSP27. Thus HSP expression can be overwhelmed by severe damage. The present work in conjunction with earlier work on caerulein induced pancreatitis indicates that changes in the actin cytoskeleton are an early component in experimental pancreatitis. (Gut 2001;49:241-250)

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Pancreatic damage induced by injecting a large dose of arginine

Cited by 33 publications

References 10 publications

Endoplasmic reticulum stress and the pancreatic acinar cell

Endoplasmic reticulum stress and the pancreatic acinar cell

Histopathological and biochemical studies on pancreatic fibrosis in WBN/Kob rats

Arginine induced acute pancreatitis alters the actin cytoskeleton and increases heat shock protein expression in rat pancreatic acinar cells

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