Changes in Cell Proliferation Produced by 12 Roentgens of 60 Co Gamma Irradiation per Day in the Intestinal Crypt Cells of 100-, 400-, and 825-Day-Old BCF 1 Mice

1967 ◽  
Vol 30 (3) ◽  
pp. 654 ◽  
Author(s):  
S. Lesher ◽  
G. A. Sacher
Keyword(s):  
Cell Proliferation ◽  
Gamma Irradiation ◽  
Intestinal Crypt ◽  
Crypt Cells

scholarly journals Glucagon-Like Peptide-2 Activates β-Catenin Signaling in the Mouse Intestinal Crypt: Role of Insulin-Like Growth Factor-I

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 291-301 ◽  
Author(s):  
Philip E. Dubé ◽  
Katherine J. Rowland ◽  
Patricia L. Brubaker
Keyword(s):  
Cell Proliferation ◽  
Nuclear Translocation ◽  
Glycogen Synthase ◽  
Crypt Cell ◽  
Acute Administration ◽  
Intestinal Crypt ◽  
Crypt Cell Proliferation ◽  
Igf I ◽  
Glucagon Like Peptide ◽  
Crypt Cells

Chronic administration of glucagon-like peptide-2 (GLP-2) induces intestinal growth and crypt cell proliferation through an indirect mechanism requiring IGF-I. However, the intracellular pathways through which IGF-I mediates GLP-2-induced epithelial tropic signaling remain undefined. Because β-catenin and Akt are important regulators of crypt cell proliferation, we hypothesized that GLP-2 activates these signaling pathways through an IGF-I-dependent mechanism. In this study, fasted mice were administered Gly2-GLP-2 or LR3-IGF-I (positive control) for 0.5–4 h. Nuclear translocation of β-catenin in non-Paneth crypt cells was assessed by immunohistochemistry and expression of its downstream proliferative markers, c-myc and Sox9, by quantitative RT-PCR. Akt phosphorylation and activation of its targets, glycogen synthase kinase-3β and caspase-3, were determined by Western blot. IGF-I receptor (IGF-IR) and IGF-I signaling were blocked by preadministration of NVP-AEW541 and through the use of IGF-I knockout mice, respectively. We found that GLP-2 increased β-catenin nuclear translocation in non-Paneth crypt cells by 72 ± 17% (P < 0.05) and increased mucosal c-myc and Sox9 mRNA expression by 90 ± 20 and 376 ± 170%, respectively (P < 0.05–0.01), with similar results observed with IGF-I. This effect of GLP-2 was prevented by blocking the IGF-IR as well as ablation of IGF-I signaling. GLP-2 also produced a time- and dose-dependent activation of Akt in the intestinal mucosa (P < 0.01), most notably in the epithelium. This action was reduced by IGF-IR inhibition but not IGF-I knockout. We concluded that acute administration of GLP-2 activates β-catenin and proliferative signaling in non-Paneth murine intestinal crypt cells as well as Akt signaling in the mucosa. However, IGF-I is required only for the GLP-2-induced alterations in β-catenin.

The preparation of isolated intestinal crypt cells

1969 ◽  
Vol 55 (2) ◽  
pp. 257-260 ◽  
Author(s):  
D.D. Harrison ◽  
H.L. Webster
Keyword(s):  
Intestinal Crypt ◽  
Crypt Cells

scholarly journals Protective effects of zingerone derivate on ionizing radiation-induced intestinal injury

2019 ◽  
Vol 60 (6) ◽  
pp. 740-746 ◽  
Author(s):  
Jing Wu ◽  
Yuqing Duan ◽  
Jie Cui ◽  
Yinping Dong ◽  
Hongyan Li ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Morphological Changes ◽  
Lethal Dose ◽  
Intestinal Injury ◽  
Intestinal Morphology ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Intestinal Crypt ◽  
Proliferation And Differentiation ◽  
Crypt Cells

Abstract Intestinal injury is the primary toxicity of radiotherapy for pelvic and abdominal tumors, and it is also one of the common acute complications of radiotherapy. At present, there are no effective drugs to prevent intestinal injury in the clinic. Zingerone is a natural product with radioprotective effects. In this study, a novel compound (thiazolidine hydrochloride, TZC01) was synthesized by structural modification of zingerone. The effects of TZC01 on preventing intestinal injury from radiation were further investigated in this study. C57BL/6N mice were exposed to a lethal dose of abdominal irradiation (ABI) with and without TZC01 treatments. The morphological changes of the intestine and various makers of intestinal crypt cells were investigated. Treatment with TZC01 improved the survival rate of mice exposed to 12 Gy ABI. Moreover, TZC01 protected the intestinal morphology of mice, decreased the apoptotic rate of intestinal crypt cells, maintained cell regeneration and promoted crypt cell proliferation and differentiation. This study suggests that TZC01 has preventive and therapeutic effects on radiation enteritis by promoting the proliferation and differentiation of crypt cells to protect the small intestine from the toxic effects of ionizing radiation. Furthermore, the study of TCZ01 lays a strong foundation for developing novel radioprotectors with multiple properties.

Amino acid and hexose transport by cultured crypt cells from rat small intestine

1980 ◽  
Vol 239 (5) ◽  
pp. C190-C196 ◽  
Author(s):  
K. Inui ◽  
A. Quaroni ◽  
L. G. Tillotson ◽  
K. J. Isselbacher
Keyword(s):  
Amino Acid ◽  
Sugar Transport ◽  
Epithelial Cell Line ◽  
Acid Uptake ◽  
Substrate Uptake ◽  
Hexose Transport ◽  
Intestinal Crypt ◽  
Morphological Criteria ◽  
Hexose Uptake ◽  
Crypt Cells

The characteristics of amino acid and sugar transport in intestinal crypt epithelial cells have been examined by measuring substrate uptake in an established epithelial cell line. These cells (IEC-6 cells) have been characterized as derived from rat small intestinal crypt cells on the basis of morphological criteria (J. Cell. Biol. 80: 248-265, 1979). Amino acid transport appeared to be mediated by both Na+-dependent and Na+-independent systems. Hexose uptake was stereospecific and Na+ independent, and was markedly inhibited by phloretin and cytochalasin B. Since glucocorticoids are known to have profound effects on maturation of the intestinal epithelium in vivo, their effects on transport properties of the cultured crypt cells were studied. Hydrocortisone, while completely inhibiting cell growth, increased the initial uptake rates of various hexoses, while having little or nor effect on the initial rate of amino acid uptake. The increased hexose uptake appeared to be due to a change in Vmax rather than Km. Appearance of the Na+-dependent hexose transport system, which is present in differentiated enterocytes, was not elicited by in vitro treatment with glucocortcoids.

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