Hyperthermia induces heat shock protein expression and protection against cerulein-induced pancreatitis in rats

Wagner, Andreas; Weber, Heike; Jonas, Ludwig; Nizze, H; Strowski, Mathias Z.; Fiedler, Fritz; Printz, H.; Steffen, Hanna; Göke, Burkhard

doi:10.1053/gast.1996.v111.pm8898648

Cited by 101 publications

(94 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The induction of Hsp70 expression prior to the onset of experimental pancreatitis in rodents protects against the zymogen activation and acinar cell damage characteristic of this clinical condition (3,43,44). In humans, pancreatitis is often resolved by preventing pancreatic stimulation via fasting, TPN, or enteral feeding (31).…”

Section: Discussionmentioning

confidence: 99%

“…In addition to Hsp70, heat shock cognate (Hsc)70 is a constitutively expressed chaperone under normal conditions that likely shares similar protein substrates (34). Interestingly, the prophylactic induction of Hsp70 was shown to have a protective effect against the onset of cerulein-induced pancreatitis (44) and arginine-induced pancreatitis (43) in rodents. Supporting this, inhibition of Hsp70 expression using antisense oligonucleotides in rat pancreatic fragments abolished its protective effects against the onset of trypsinogen activation in response to cerulein hyperstimulation, which is believed to cause pancreatitis (3).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Loss of exocrine pancreatic stimulation during parenteral feeding suppresses digestive enzyme expression and induces Hsp70 expression

Baumler

Nelson²,

Ney³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Luminal nutrients are essential for the growth and maintenance of digestive tissue including the pancreas and small intestinal mucosa. Long-term loss of luminal nutrients such as during animal hibernation has been shown to result in mucosal atrophy and a corresponding stress response characterized by the induction of heat shock protein (Hsp)70 expression. This study was conducted to determine if the loss of luminal nutrients during total parenteral nutrition (TPN) would result in atrophy of the exocrine pancreas and small intestinal mucosa as well as an induction of Hsp70 expression in rats. In experiment 1, the treatment groups included an orally fed control, a saline-infused surgical control, or TPN treatment for 7 days. In experiment 2, the treatment groups included an orally fed control and TPN alone or coinfused with varying doses of glucagon-like peptide (GLP)-2, a mucosal proliferation agent, for 7 days. In experiment 1, TPN resulted in a 40% reduction in pancreatic mass that was associated with a dramatic reduction in digestive enzyme expression, enhanced apoptosis, and a 200% increase in Hsp70 expression. Conversely, heat shock cognate 70, Hsp27, and Hsp60 expression was not changed in the pancreas. In experiment 2, TPN resulted in a 30% reduction in jejunal mucosa mass and a similar induction of Hsp70 expression. The inclusion of GLP-2 during TPN attenuated jejunal mucosal atrophy and inhibited Hsp70 expression, suggesting that Hsp70 induction is sensitive to cell growth. These data indicate that pancreatic and intestinal mucosal atrophy caused by a loss of luminal nutrient stimulation is accompanied by a compensatory response involving Hsp70.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Loss of exocrine pancreatic stimulation during parenteral feeding suppresses digestive enzyme expression and induces Hsp70 expression

Baumler

Nelson²,

Ney³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…Another suggestion is that hyperthermia might directly prevent the activation of pancreatic enzymes; however, another report showed that kinase activation activity was unaltered after heating procedure (24) ; nevertheless, this issue is controversial and other studies had demonstrated opposite results (4,13) . Another explanation is that the protective effect afforded by hyperthermia could be mediated by HSPs ("heat shock proteins") (35,37) . It is believed that HSPs act as molecular chaperones, making the fi nal folding of other proteins easier and protecting them from additional injuries.…”

Section: Resultsmentioning

confidence: 99%

“…It is believed that HSPs act as molecular chaperones, making the fi nal folding of other proteins easier and protecting them from additional injuries. Several reports had showed that when hyperthermia is performed before induction of AP, the lesion caused by cerulein is diminished (37) .…”

Section: Resultsmentioning

confidence: 99%

Effect of hyperthermia on experimental acute pancreatitis

Almeida

Jukemura

Sampietre

et al. 2006

Arq. Gastroenterol.

View full text Add to dashboard Cite

-Background -Recent studies indicate that hyperthermia can change infl ammatory mechanisms and protect experimental animals from deleterious effects of secretagogue-induced acute pancreatitis. Aim -To evaluate the effects of hyperthermia posttreatment on cerulein-induced acute pancreatitis in rats. Methods -Twenty animals were divided in two groups: group I (n = 10), rats with cerulein-induced acute pancreatitis undergone hyperthermia, and group II (n = 10), animals with cerulein-induced acute pancreatitis that were kept normothermic. In all groups, amylase serum levels, histologic damage, vascular permeability and pancreatic water content were assessed. Acute pancreatitis was induced by administration of two cerulein injections (20 mcg/kg). A single dose of Evans' blue dye was administered along with the second dose of cerulein. All animals also received a subcutaneous injection of saline solution. After this process, animals undergone hyperthermia were heated in a cage with two 100 W lamps. Body temperature was increased to 39.5ºC and maintained at that level for 45 minutes. Normothermia rats were kept at room temperature in a second cage. Results -Control animals had typical edema, serum amylase activity and morphologic changes of this acute pancreatitis model. Hyperthermia post-treatment ameliorated the pancreatic edema, whereas the histologic damage and the serum amylase level remained unchanged. Conclusions -The fi ndings suggest a benefi cial effect of the thermal stress on infl ammatory edema in experimental acute pancreatitis.

show abstract

“…HSPs are induced by a variety of stresses, including heat, free radicals, and toxins [16] . In the pancreas, HSPs have been shown to provide the protection against cerulein- [17,18] and arginine-induced [19] acute pancreatitis. However, it is not investigated whether IP interacts with HSPs and what is the biological consequence of this potential interaction in the development of cerulein-induced pancreatitis.…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

Ischemic preconditioning inhibits development of edematous cerulein-induced pancreatitis: Involvement of cyclooxygenases and heat shock protein 70

Warzecha

Dembiński²,

Ceranowicz³

et al. 2005

WJG

View full text Add to dashboard Cite

Abstract Abstract Abstract AIM: To determine whether ischemic preconditioning (IP) affects the development of edematous cerulein-induced pancreatitis and to assess the role of cyclooxygenase-1 (COX-1), COX-2, and heat shock protein 70 (HSP 70) in this process. METHODS:In male Wistar rats, IP was performed by clamping of celiac artery (twice for 5 min at 5-min intervals). Thirty minutes after IP or sham operation, acute pancreatitis was induced by cerulein. Activity of COX-1 or COX-2 was inhibited by resveratrol or rofecoxib, respectively (10 mg/kg). RESULTS:IP significantly reduced pancreatic damage in cerulein-induced pancreatitis as demonstrated by the improvement of pancreas histology, reduction in serum lipase and poly-C ribonuclease activity, and serum concentration of pro-inflammatory interleukin (IL)-1β. Also, IP attenuated the pancreatitis-evoked fall in pancreatic blood flow and pancreatic DNA synthesis. Serum level of anti-inflammatory IL-10 was not affected by IP. Cerulein-induced pancreatitis and IP increased the content of HSP 70 in the pancreas. Maximal increase in HSP 70 was observed when IP was combined with cerulein-induced pancreatitis. Inhibition of COXs, especially COX-2, reduced the protective effect of IP in edematous pancreatitis. CONCLUSION:Our results indicate that IP reduces pancreatic damage in cerulein-induced pancreatitis and this effect, at least in part, depends on the activity of COXs and pancreatic production of HSP 70.

show abstract

Hyperthermia induces heat shock protein expression and protection against cerulein-induced pancreatitis in rats

Cited by 101 publications

References 0 publications

Loss of exocrine pancreatic stimulation during parenteral feeding suppresses digestive enzyme expression and induces Hsp70 expression

Loss of exocrine pancreatic stimulation during parenteral feeding suppresses digestive enzyme expression and induces Hsp70 expression

Effect of hyperthermia on experimental acute pancreatitis

Ischemic preconditioning inhibits development of edematous cerulein-induced pancreatitis: Involvement of cyclooxygenases and heat shock protein 70

Contact Info

Product

Resources

About