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Interleukin-10 up-regulates tumour-necrosis-factor-alpha-related apoptosis-inducing ligand (TRAIL) gene expression in mammary epithelial cells at the involution stage

Title
Interleukin-10 up-regulates tumour-necrosis-factor-alpha-related apoptosis-inducing ligand (TRAIL) gene expression in mammary epithelial cells at the involution stage
Authors
Sohn, BHMoon, HBKim, TYKang, HSBae, YSLee, KKKim, SJ
Ewha Authors
배윤수
SCOPUS Author ID
배윤수scopus
Issue Date
2001
Journal Title
BIOCHEMICAL JOURNAL
ISSN
0264-6021JCR Link
Citation
vol. 360, pp. 31 - 38
Keywords
apoptosisdeath receptormammary gland
Publisher
PORTLAND PRESS
Indexed
SCI; SCIE; SCOPUS WOS
Abstract
Although interleukin-10 (IL-10) is known to contribute to inflammation and pathogenesis in mammalian organs, little is known about its precise role in the mammary gland. We found that IL-10 levels fluctuated during the mouse mammary cycle, showing little expression at the lactation stage and the highest expression at the involution stage. To reveal the effects of IL-10 on involution, expression profiles of apoptosis-related genes were examined in mice transgenic for IL-10 as well as in IL-10(-/-) mice. Mild inflammatory lesions by lymphocytes were observed in the mammary glands from four of seven transgenic lines at the lactation stage. It was striking that the expression of tumour-necrosis-factor-alpha -related apoptosis-inducing ligand (TRAIL) among the apoptosis-related genes was elevated approx. 7-fold in the transgenic mice, whereas others were almost unchanged. Furthermore, TRAIL was down-regulated 4-fold in the IL-10(-/-) mice at the involution stage. Elevated expression of TRAIL and of death receptor 4 (DR4) protein was identified at the involution stage of normal mammary glands as well as at the lactation stage of the IL-10 transgenic mice. These results indicate that the elevated expression of IL-10 at the involution stage recruits lymphocytes and induces the expression of TRAIL and DR4. These phenomena might partly contribute to apoptosis in the mammary epithelial cells for entering involution.
DOI
10.1042/0264-6021:3600031
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자연과학대학 > 생명과학전공 > Journal papers
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