Increased heat shock protein 70 expression attenuates pancreatic fibrosis induced by dibutyltin dichloride

Research output: Contribution to journalArticle

Abstract

Objectives: Heat shock protein (HSP) 70 performs a chaperoning function and protects cells against injury. Although the effect of HSPs against acute inflammatory change has been proven, the relationship between HSP70 and chronic pancreatitis remains unclear. This study aimed to investigate the protective effect of increased HSP70 expression induced by thermal stress against pancreatic fibrosis in experimental chronic pancreatitis. Materials and Methods: Two experiments to evaluate pancreatic HSP70 expression induced by thermal stress and determine the effect of increased HSP70 expression against pancreatic fibrosis were performed. To investigate HSP70 expression, rats were immersed in a warm bath and sequentially killed, and pancreatic HSP70 expression was measured. To study the effect of increased HSP70 expression, pancreatic fibrosis was induced by intravenous injection of dibutyltin dichloride (DBTC) and analyzed under repeated thermal stress. The severity of pancreatic fibrosis was measured. Results: Thermal stress significantly increased HSP70 expression in the pancreas. HSP70 expression peaked at 6–12 h after warm bathing, and the increased HSP70 expression was associated with the attenuation of pancreatic fibrosis. Although pancreatic fibrosis was induced by DBTC injection, HSP70 expression induced by repeated thermal stress diminished the severity of atrophy and fibrosis. On western blot analysis, collagen type 1 expression was diminished in the increased HSP70 expression group, but not α-smooth muscle actin expression. Conclusions: Thermal stress could increase pancreatic HSP70 expression, and induced HSP70 expression showed a protective effect against pancreatic fibrosis. Modulation of HSP70 expression could be a potential therapeutic target in the treatment of chronic pancreatitis.

Original languageEnglish
JournalScandinavian Journal of Gastroenterology
DOIs
Publication statusAccepted/In press - 2018 Jan 1

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HSP70 Heat-Shock Proteins
Fibrosis
Hot Temperature
Chronic Pancreatitis
dibutyldichlorotin
Collagen Type I
Baths
Intravenous Injections
Atrophy
Smooth Muscle
Actins
Pancreas
Western Blotting
Injections
Wounds and Injuries
Therapeutics

Keywords

  • Chronic pancreatitis
  • dibutyltin dichloride
  • heat shock protein
  • pancreatic fibrosis

ASJC Scopus subject areas

  • Gastroenterology

Cite this

@article{48798448221f4089bc539e712693d637,
title = "Increased heat shock protein 70 expression attenuates pancreatic fibrosis induced by dibutyltin dichloride",
abstract = "Objectives: Heat shock protein (HSP) 70 performs a chaperoning function and protects cells against injury. Although the effect of HSPs against acute inflammatory change has been proven, the relationship between HSP70 and chronic pancreatitis remains unclear. This study aimed to investigate the protective effect of increased HSP70 expression induced by thermal stress against pancreatic fibrosis in experimental chronic pancreatitis. Materials and Methods: Two experiments to evaluate pancreatic HSP70 expression induced by thermal stress and determine the effect of increased HSP70 expression against pancreatic fibrosis were performed. To investigate HSP70 expression, rats were immersed in a warm bath and sequentially killed, and pancreatic HSP70 expression was measured. To study the effect of increased HSP70 expression, pancreatic fibrosis was induced by intravenous injection of dibutyltin dichloride (DBTC) and analyzed under repeated thermal stress. The severity of pancreatic fibrosis was measured. Results: Thermal stress significantly increased HSP70 expression in the pancreas. HSP70 expression peaked at 6–12 h after warm bathing, and the increased HSP70 expression was associated with the attenuation of pancreatic fibrosis. Although pancreatic fibrosis was induced by DBTC injection, HSP70 expression induced by repeated thermal stress diminished the severity of atrophy and fibrosis. On western blot analysis, collagen type 1 expression was diminished in the increased HSP70 expression group, but not α-smooth muscle actin expression. Conclusions: Thermal stress could increase pancreatic HSP70 expression, and induced HSP70 expression showed a protective effect against pancreatic fibrosis. Modulation of HSP70 expression could be a potential therapeutic target in the treatment of chronic pancreatitis.",
keywords = "Chronic pancreatitis, dibutyltin dichloride, heat shock protein, pancreatic fibrosis",
author = "Lee, {Jae Min} and Lee, {Kwang Gyun} and Choi, {Hyuk Soon} and Eun-Sun Kim and Bora Keum and Seo, {Yeon Seok} and Jeen, {Yoon Tae} and Hoon-Jai Chun and Lee, {Hong Sik} and Soon-Ho Um and Kim, {Chang Duck}",
year = "2018",
month = "1",
day = "1",
doi = "10.1080/00365521.2018.1516799",
language = "English",
journal = "Scandinavian Journal of Gastroenterology",
issn = "0036-5521",
publisher = "Informa Healthcare",

}

TY - JOUR

T1 - Increased heat shock protein 70 expression attenuates pancreatic fibrosis induced by dibutyltin dichloride

AU - Lee, Jae Min

AU - Lee, Kwang Gyun

AU - Choi, Hyuk Soon

AU - Kim, Eun-Sun

AU - Keum, Bora

AU - Seo, Yeon Seok

AU - Jeen, Yoon Tae

AU - Chun, Hoon-Jai

AU - Lee, Hong Sik

AU - Um, Soon-Ho

AU - Kim, Chang Duck

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Objectives: Heat shock protein (HSP) 70 performs a chaperoning function and protects cells against injury. Although the effect of HSPs against acute inflammatory change has been proven, the relationship between HSP70 and chronic pancreatitis remains unclear. This study aimed to investigate the protective effect of increased HSP70 expression induced by thermal stress against pancreatic fibrosis in experimental chronic pancreatitis. Materials and Methods: Two experiments to evaluate pancreatic HSP70 expression induced by thermal stress and determine the effect of increased HSP70 expression against pancreatic fibrosis were performed. To investigate HSP70 expression, rats were immersed in a warm bath and sequentially killed, and pancreatic HSP70 expression was measured. To study the effect of increased HSP70 expression, pancreatic fibrosis was induced by intravenous injection of dibutyltin dichloride (DBTC) and analyzed under repeated thermal stress. The severity of pancreatic fibrosis was measured. Results: Thermal stress significantly increased HSP70 expression in the pancreas. HSP70 expression peaked at 6–12 h after warm bathing, and the increased HSP70 expression was associated with the attenuation of pancreatic fibrosis. Although pancreatic fibrosis was induced by DBTC injection, HSP70 expression induced by repeated thermal stress diminished the severity of atrophy and fibrosis. On western blot analysis, collagen type 1 expression was diminished in the increased HSP70 expression group, but not α-smooth muscle actin expression. Conclusions: Thermal stress could increase pancreatic HSP70 expression, and induced HSP70 expression showed a protective effect against pancreatic fibrosis. Modulation of HSP70 expression could be a potential therapeutic target in the treatment of chronic pancreatitis.

AB - Objectives: Heat shock protein (HSP) 70 performs a chaperoning function and protects cells against injury. Although the effect of HSPs against acute inflammatory change has been proven, the relationship between HSP70 and chronic pancreatitis remains unclear. This study aimed to investigate the protective effect of increased HSP70 expression induced by thermal stress against pancreatic fibrosis in experimental chronic pancreatitis. Materials and Methods: Two experiments to evaluate pancreatic HSP70 expression induced by thermal stress and determine the effect of increased HSP70 expression against pancreatic fibrosis were performed. To investigate HSP70 expression, rats were immersed in a warm bath and sequentially killed, and pancreatic HSP70 expression was measured. To study the effect of increased HSP70 expression, pancreatic fibrosis was induced by intravenous injection of dibutyltin dichloride (DBTC) and analyzed under repeated thermal stress. The severity of pancreatic fibrosis was measured. Results: Thermal stress significantly increased HSP70 expression in the pancreas. HSP70 expression peaked at 6–12 h after warm bathing, and the increased HSP70 expression was associated with the attenuation of pancreatic fibrosis. Although pancreatic fibrosis was induced by DBTC injection, HSP70 expression induced by repeated thermal stress diminished the severity of atrophy and fibrosis. On western blot analysis, collagen type 1 expression was diminished in the increased HSP70 expression group, but not α-smooth muscle actin expression. Conclusions: Thermal stress could increase pancreatic HSP70 expression, and induced HSP70 expression showed a protective effect against pancreatic fibrosis. Modulation of HSP70 expression could be a potential therapeutic target in the treatment of chronic pancreatitis.

KW - Chronic pancreatitis

KW - dibutyltin dichloride

KW - heat shock protein

KW - pancreatic fibrosis

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U2 - 10.1080/00365521.2018.1516799

DO - 10.1080/00365521.2018.1516799

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JO - Scandinavian Journal of Gastroenterology

JF - Scandinavian Journal of Gastroenterology

SN - 0036-5521

ER -