Rapid Apoptotic Changes in the Gastric Glandular Epithelium of Rats Administered Intraperitoneally with Fusarenon-X.

Li, Jinjun; Shimizu, Tsutomu; Miyoshi, Noriaki; Yasuda, Nobuhiro

doi:10.1292/jvms.59.17

Cited by 6 publications

(10 citation statements)

References 14 publications

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“…By these two methods we obtained high TI and AI values after 3 hr of hydrocortisone treatment, suggesting that the activation of the death process is rapid. Li et al (1997) also verified that in rats treated with Fusarenon-X, the apoptotic peak occurred 3 hr after treatment. These results are in agreement with Grossmann et al (1998), who showed that the activation of intestinal caspases starts after a few minutes of induction and DNA fragmentation happens in 2 hr.…”

Section: Discussionsupporting

confidence: 67%

“…The differential distribution of apoptotic cells along the gastric mucosa was observed either after the TUNEL reaction or the morphological study. Li et al (1997) recorded a higher number of dead cells at the bottom of the gland, that were identified as chief cells by electron microscopy. This same study also showed that parietal cells phagocytosed the apoptotic ones.…”

Section: Discussionmentioning

confidence: 97%

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Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

et al. 2000

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Glucocorticoids take part in the intense morphofunctional modifications that occur in the gastric mucosa during fetal and postnatal development. Two studies were designed to evaluate corticoids role in gastric cell proliferation and apoptosis in developing rats: in vivo, using suckling animals; in vitro, using gastric explants obtained from 20-day fetuses. These explants were cultured in DMEM/F12 medium treated or not with 50 ng/ml of corticosterone; after 22 hr, vincristine was added to the medium for 2 hr to block mitosis. The metaphasic index decreased significantly after the 24-hr treatment (controls: 1.52 +/- 0.53; treated: 0.40 +/- 0.21) and apoptotic cells were visualized under light and electron microscopy. Fifteen-day-old rats were treated with hydrocortisone (25 mg/Kg) for 3 days, and injected with BrDU (100 mg/Kg) 1 hr before sacrifice on the 18th day. BrDu-labeled and non-labeled cells were counted to determine the labeling index of epithelial cells. As apoptotic cells are rapidly eliminated, other animals were treated for only 2-3 hr. Sections were investigated for the presence of apoptotic cells, using morphological criteria and TUNEL labeling. Hydrocortisone significantly reduced the labeling index (controls: 15.6 +/- 1.6 vs. treated: 11.7 +/- 1.1), besides altering the body weight gain. Hydrocortisone treatment doubled the number of apoptotic cells after 2 hr, and quadruplicated it after 3 hr. The results demonstrated that glucocorticoids inhibit cell proliferation in the gastric epithelium of fetuses and suckling rats and increase apoptotic rates, suggesting the exit from cell cycle.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 97%

Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

et al. 2000

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“…As found for COX-2, DON can stabilize mRNAs for TNF-α (Chung et al 2003b; Chung et al 2003a) and IL-6 (Jia et al 2006) in macrophages as well as IL-2 in EL-4 T cells, (Li et al 1997a; Li et al 1997b; Li et al 1997c; Li et al 1997d; Li et al 1997e). Contrastingly, mRNA stabilization dose not play a role in DON-induced IL-8 in monocytes (Gray and Pestka, 2007, in press).…”

Section: Molecular Mechanisms For Trichothecene-mediated Immune Dysrementioning

confidence: 62%

Mechanisms of deoxynivalenol-induced gene expression and apoptosis

Pestka

2008

Food Additives & Contaminants: Part A

251

187

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Fusarium infection of agricultural staples such as wheat, barley and corn with concurrent production of deoxynivalenol (DON) and other trichothecene mycotoxins is an increasingly common problem worldwide. In addition to its emetic effects, chronic dietary exposure to DON causes impaired weight gain, anorexia, decreased nutritional efficiency and immune dysregulation in experimental animals. Trichothecenes are both immunostimulatory or immunosuppressive depending on dose, frequency and duration of exposure as well as type of immune function assay. Monocytes, macrophages, as well as T and B lymphocytes of the immune system can be cellular targets of DON and other trichothecenes. In vitro exposure to low trichothecene concentrations upregulates expression both transcriptionally and post-transcriptionally of cytokines, chemokines and inflammatory genes with concurrent immune stimulation, whereas exposure to high concentrations promotes leukocyte apoptosis with concomitant immune suppression. DON and other trichothecenes, via a mechanism known as the "ribotoxic stress response", bind to ribosomes and rapidly activate mitogen-activated protein kinases (MAPKs). The latter are important transducers of downstream signaling events related to immune response and apoptosis. Using cloned macrophages, we have identified two critical upstream transducers of DON-induced MAPK activation. One transducer is double-stranded RNA-(dsRNA)-activated protein kinase (PKR), a widely-expressed serine/theonine protein kinase that can be activated by dsRNA, interferon and other agents. The other transducer is hematopoetic cell kinase (Hck), a non-receptor associated Src oncogene family kinase. Pharmacologic inhibitors and gene suppression studies have revealed that Hck and PKR contribute to DON-induced gene expression and apoptosis. PKR, Hck and other kinases bind to the ribosome and are activated following DON interaction. Future studies will focus on the sequence of molecular events at the ribosome level that drive selective activation of these upstream kinases.

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“…By these two methods we obtained high TI and AI values after 3 hr of hydrocortisone treatment, suggesting that the activation of the death process is rapid. Li et al (1997) also verified that in rats treated with Fusarenon‐X, the apoptotic peak occurred 3 hr after treatment. These results are in agreement with Grossmann et al (1998), who showed that the activation of intestinal caspases starts after a few minutes of induction and DNA fragmentation happens in 2 hr.…”

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

et al. 2000

View full text Add to dashboard Cite

Glucocorticoids take part in the intense morphofunctional modifications that occur in the gastric mucosa during fetal and postnatal development. Two studies were designed to evaluate corticoids role in gastric cell proliferation and apoptosis in developing rats: in vivo, using suckling animals; in vitro, using gastric explants obtained from 20‐day fetuses. These explants were cultured in DMEM/F12 medium treated or not with 50 ng/ml of corticosterone; after 22 hr, vincristine was added to the medium for 2 hr to block mitosis. The metaphasic index decreased significantly after the 24‐hr treatment (controls: 1.52 ± 0.53; treated: 0.40 ± 0.21) and apoptotic cells were visualized under light and electron microscopy. Fifteen‐day‐old rats were treated with hydrocortisone (25 mg/Kg) for 3 days, and injected with BrDU (100 mg/Kg) 1 hr before sacrifice on the 18th day. BrDu‐labeled and non‐labeled cells were counted to determine the labeling index of epithelial cells. As apoptotic cells are rapidly eliminated, other animals were treated for only 2–3 hr. Sections were investigated for the presence of apoptotic cells, using morphological criteria and TUNEL labeling. Hydrocortisone significantly reduced the labeling index (controls: 15.6 ± 1.6 vs. treated: 11.7 ± 1.1), besides altering the body weight gain. Hydrocortisone treatment doubled the number of apoptotic cells after 2 hr, and quadruplicated it after 3 hr. The results demonstrated that glucocorticoids inhibit cell proliferation in the gastric epithelium of fetuses and suckling rats and increase apoptotic rates, suggesting the exit from cell cycle. Anat Rec 260:213–221, 2000. © 2000 Wiley‐Liss, Inc.

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Rapid Apoptotic Changes in the Gastric Glandular Epithelium of Rats Administered Intraperitoneally with Fusarenon-X.

Cited by 6 publications

References 14 publications

Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

Mechanisms of deoxynivalenol-induced gene expression and apoptosis

Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

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