Induction of a 60-kDa heat shock protein in rat gastric mucosa by restraint and water-immersion stress

Fujimori, Shusei; Otaka, Michiro; Kuwabara, Toshiyuki; Zeniya, Akira; Otani, Setsuya; Tashima, Yohtalou; Masamune, Osamu

doi:10.1007/bf02361257

Cited by 11 publications

(8 citation statements)

References 10 publications

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“…2007). Mammalian Hsps has induced by various ambient temperatures or environments in vivo (Fujimori et al 1994;Kim et al 2004). Transportation is thought to be very stressful due to exposure of the animals to unfavorable environments.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that, 12 h after the initiation of water-immersion stress, rats were found to have acute gastric mucosal lesions and Hsp60 levels were significantly higher than that of the control rats (Fujimori et al 1994). Sleep deprivation was also considered as a stressor, with partial sleep deprivation producing gastric lesions in the corpus or pylorus of the stomach in approximately 30-50% of the experimental rats (Guo et al 2005).…”

Section: Discussionmentioning

confidence: 99%

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Expression of heat shock protein 60 in the tissues of transported piglets

Zhu

Bao

Zhao

et al. 2009

Cell Stress and Chaperones

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In this study, we sought to determine the distribution and expression of heat shock protein 60 (Hsp60) in the tissues of transported piglets. A total of 24 Chinese Erhualian piglets with an average body weight of 20±1 kg were assessed under both 2-h transported and normal housing conditions. Results of enzymatic analysis showed that the serum creatine kinase and aspartate aminotransferase concentrations were significantly increased in the 2-h transported piglets. Acute cellular lesions characterized by granular and vacuolar degeneration of the parenchyma cells in the tested heart, liver, and kidney were also confirmed by histopathological test after 2 h transportation. These results indicate that transport stress induces tissue damage to heart, liver, and kidney. Hsp60-positive immunostaining was consistently detected in the cytoplasm of myocardial cells, hepatocytes, renal tubular epithelial cells, and epithelial cells of fundic gland. However, results of enzyme-linked immunosorbent assay indicated that Hsp60 expression was only significantly elevated in the stomach, with lower expression in the heart and a nonsignificant trend of increased liver and kidney expression of Hsp60. These results indicate that different tissues had different sensitivities to transport stress, possibly resulting in varying levels of cytoprotection by Hsp60 in the different tissues. The expression of Hsp60 following 2 h transportation coincided with deterioration of cardiac cytoprotection in the heart and protection in the stomach. However, the direct role of Hsp60 in cytoprotection of heart and stomach tissues needs further investigation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression of heat shock protein 60 in the tissues of transported piglets

Zhu

Bao

Zhao

et al. 2009

Cell Stress and Chaperones

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“…[15][16][17][18] Recent attention has also been focused on the relationship between HSPs and adaptive cytoprotection. 4,19,20 Yeomans et al 21 reported that HSPs were expressed as a result of cellular damage in rats with injury to the gastric mucosa induced by diclofenac; however, they indicated that the expression of HSPs was probably not the principal mechanism of adaptation. Furthermore, the expression of cyclooxygenase-2 (Cox-2), a rate-limiting enzyme in prostaglandin synthesis, has attracted recent attention in relation to cytoprotection of the gastric mucosa.…”

Section: Discussionmentioning

confidence: 95%

Injury to the Gastric Mucosa and Cellular Dynamics in a Rat Model of Duodenogastric Reflux: The Possible Significance of Gastrin Induction and a Heat Shock Protein

Kubo¹,

Noguchi²,

Takeno³

et al. 2000

Surgery Today

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Injury to the gastric mucosa caused by duodenogastric reflux (DGR) is often encountered after gastrectomy or truncal vagotomy (V) with pyloroplasty. This study was designed to investigate the histological features of the gastric mucosa under such conditions. A rat model of DGR and DGR+V was established and the thickness of the oxyntic mucosa was measured. Cellular dynamics in the presence of injury to the gastric mucosa caused by DGR were investigated by the immunohistochemical staining of bromodeoxyuridine (BrdU) and heat shock protein 70 (HSP70). The relationship between persistent hypergastrinemia and mucosal injury was also studied. Duodenogastric reflux activated the intracellular induction of HSP70 in our rat model of DGR. Hypergastrinemia was noted in the V group. Compared with values from the DGR group, the numbers of BrdU-labeled cells increased, the glandular proliferation zone expanded, and the thickness of the oxyntic mucosa was significantly higher in the DGR+V group. Compared with the DGR group, there was greater induction of HSP in the DGR+V group during the acute stage. This finding suggests that denervation of the gastric mucosa and hypergastrinemia after vagotomy may be associated with the expression of HSP.

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“…Many reports have suggested cytoprotective ability of HSPs in the gastrointestinal mucosa. As the mechanism for HSP induction in the gastrointestinal mucosa, it has been reported that hyperthermia, mild irritation (gastric acid, zinc) and secondaryinduced ischaemic conditions (water-immersion stress, serotonin, thyrotropin-releasing hormone) could be important factors [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Although some precise mechanisms are still uncertain, especially in vivo, some possible mechanisms are summarised based on the mode of action of stressors in Table I.…”

Section: Protection Of Gastrointestinal Mucosa By Hsp Inductionmentioning

confidence: 99%

“…Our recent studies have focused on the 'chaperone' function of HSPs mainly their cytoprotective functions in digestive organs and cells [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. In this series of studies, we have demonstrated that (1) HSPs are induced by several environmental stresses including heat, neuropeptide, neuroamine or drugs also in vivo; (2) induced HSPs are different even by same stress in each organ; (3) in view of cytoprotection, important HSPs are different in each organ.…”

Section: Introductionmentioning

confidence: 99%

Expression and function of stress (heat shock) proteins in gastrointestinal tract

Otaka

Odashima

Tamaki

et al. 2009

International Journal of Hyperthermia

Self Cite

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This review will focus on gastrointestinal mucosal protection against cytotoxic agents and cellular stress mainly from the viewpoint of expression and function of heat shock proteins, in their role of 'molecular chaperones', as internal cytoprotectants. Also, recently identified target molecules of heat shock protein in damaged gastric mucosal cells are introduced. Elucidation of such stress-responses and repairing process of damaged protein by heat shock proteins in the gastrointestinal mucosa may provide a better understanding for the mechanisms of cytoprotection and cellular repair. In addition, these findings in post-genomic level may provide new strategies for the therapy of gastrointestinal disorders.

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Induction of a 60-kDa heat shock protein in rat gastric mucosa by restraint and water-immersion stress

Cited by 11 publications

References 10 publications

Expression of heat shock protein 60 in the tissues of transported piglets

Expression of heat shock protein 60 in the tissues of transported piglets

Injury to the Gastric Mucosa and Cellular Dynamics in a Rat Model of Duodenogastric Reflux: The Possible Significance of Gastrin Induction and a Heat Shock Protein

Expression and function of stress (heat shock) proteins in gastrointestinal tract

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