Water Immersion Stress Prevents Caerulein-induced Pancreatic Acinar Cell NF-κB Activation by Attenuating Caerulein-induced Intracellular Ca 2+ Changes

Antti J. Hietaranta, Vijay Prem Singh, Lakshmi Bhagat, Gijs J D Van Acker, Albert M. Song, Andreas Mykoniatis, Michael L. Steer, Ashok K. Saluja

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Prior stress ameliorates caerulein-induced pancreatitis in rats. NF-κB is a proinflammatory transcription factor activated during caerulein pancreatitis. However, the effects of prior stress on pancreatic NF-κB activation are unknown. In the current study, the effect of prior water immersion stress on caerulein and tumor necrosis factor-α (TNF-α)-induced NF-κB activation in the pancreas was evaluated. Water immersion of rats for up to 6 h prevents supramaximal caerulein-induced pancreatic IκB-α degradation and NF-κB activation in vivo. NF-κB activity is also inhibited in vitro in pancreatic acini prepared from water-immersed animals. TNF-α-induced NF-κB activation in pancreas or in pancreatic acini is unaffected by prior water immersion. Chelation of intracellular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetate/acetoxymethyl ester has similar effects to water immersion in preventing caerulein but not TNF-α-induced NF-κB activation in pancreas. Both the spike response and the sustained rise in [Ca2+]i in response to supramaximal caerulein stimulation are reduced markedly in acini prepared from water-immersed animals as compared with normal animals. Our findings indicate that, in addition to Ca2+-dependent mechanisms, Ca 2+-independent signaling events also may lead to NF-κB activation in pancreatic acinar cells. Water immersion stress prevents supramaximal caerulein-induced NF-κB activation in pancreas in vivo and in vitro by affecting intracellular Ca2+ homeostasis.

Original languageEnglish (US)
Pages (from-to)18742-18747
Number of pages6
JournalJournal of Biological Chemistry
Volume276
Issue number22
DOIs
StatePublished - Jun 1 2001
Externally publishedYes

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Ceruletide
Acinar Cells
Immersion
Dehydration
Chemical activation
Water
Pancreas
Animals
Tumor Necrosis Factor-alpha
Pancreatitis
Rats
Ethane
Chelation
Esters
Homeostasis
Transcription Factors
Degradation

ASJC Scopus subject areas

  • Biochemistry

Cite this

Water Immersion Stress Prevents Caerulein-induced Pancreatic Acinar Cell NF-κB Activation by Attenuating Caerulein-induced Intracellular Ca 2+ Changes. / Hietaranta, Antti J.; Singh, Vijay Prem; Bhagat, Lakshmi; Van Acker, Gijs J D; Song, Albert M.; Mykoniatis, Andreas; Steer, Michael L.; Saluja, Ashok K.

In: Journal of Biological Chemistry, Vol. 276, No. 22, 01.06.2001, p. 18742-18747.

Research output: Contribution to journalArticle

Hietaranta, Antti J. ; Singh, Vijay Prem ; Bhagat, Lakshmi ; Van Acker, Gijs J D ; Song, Albert M. ; Mykoniatis, Andreas ; Steer, Michael L. ; Saluja, Ashok K. / Water Immersion Stress Prevents Caerulein-induced Pancreatic Acinar Cell NF-κB Activation by Attenuating Caerulein-induced Intracellular Ca 2+ Changes. In: Journal of Biological Chemistry. 2001 ; Vol. 276, No. 22. pp. 18742-18747.
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abstract = "Prior stress ameliorates caerulein-induced pancreatitis in rats. NF-κB is a proinflammatory transcription factor activated during caerulein pancreatitis. However, the effects of prior stress on pancreatic NF-κB activation are unknown. In the current study, the effect of prior water immersion stress on caerulein and tumor necrosis factor-α (TNF-α)-induced NF-κB activation in the pancreas was evaluated. Water immersion of rats for up to 6 h prevents supramaximal caerulein-induced pancreatic IκB-α degradation and NF-κB activation in vivo. NF-κB activity is also inhibited in vitro in pancreatic acini prepared from water-immersed animals. TNF-α-induced NF-κB activation in pancreas or in pancreatic acini is unaffected by prior water immersion. Chelation of intracellular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetate/acetoxymethyl ester has similar effects to water immersion in preventing caerulein but not TNF-α-induced NF-κB activation in pancreas. Both the spike response and the sustained rise in [Ca2+]i in response to supramaximal caerulein stimulation are reduced markedly in acini prepared from water-immersed animals as compared with normal animals. Our findings indicate that, in addition to Ca2+-dependent mechanisms, Ca 2+-independent signaling events also may lead to NF-κB activation in pancreatic acinar cells. Water immersion stress prevents supramaximal caerulein-induced NF-κB activation in pancreas in vivo and in vitro by affecting intracellular Ca2+ homeostasis.",
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AU - Singh, Vijay Prem

AU - Bhagat, Lakshmi

AU - Van Acker, Gijs J D

AU - Song, Albert M.

AU - Mykoniatis, Andreas

AU - Steer, Michael L.

AU - Saluja, Ashok K.

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N2 - Prior stress ameliorates caerulein-induced pancreatitis in rats. NF-κB is a proinflammatory transcription factor activated during caerulein pancreatitis. However, the effects of prior stress on pancreatic NF-κB activation are unknown. In the current study, the effect of prior water immersion stress on caerulein and tumor necrosis factor-α (TNF-α)-induced NF-κB activation in the pancreas was evaluated. Water immersion of rats for up to 6 h prevents supramaximal caerulein-induced pancreatic IκB-α degradation and NF-κB activation in vivo. NF-κB activity is also inhibited in vitro in pancreatic acini prepared from water-immersed animals. TNF-α-induced NF-κB activation in pancreas or in pancreatic acini is unaffected by prior water immersion. Chelation of intracellular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetate/acetoxymethyl ester has similar effects to water immersion in preventing caerulein but not TNF-α-induced NF-κB activation in pancreas. Both the spike response and the sustained rise in [Ca2+]i in response to supramaximal caerulein stimulation are reduced markedly in acini prepared from water-immersed animals as compared with normal animals. Our findings indicate that, in addition to Ca2+-dependent mechanisms, Ca 2+-independent signaling events also may lead to NF-κB activation in pancreatic acinar cells. Water immersion stress prevents supramaximal caerulein-induced NF-κB activation in pancreas in vivo and in vitro by affecting intracellular Ca2+ homeostasis.

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