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Premature mammary gland involution with repeated corticosterone injection in interleukin 10-deficient mice
IL-10 is important for stress modulation, and impaired IL-10 function can cause premature mammary gland involution and pup alopecia. Recently, we found that maternal stress could induce premature mammary gland involution in interleukin 10 knock out (IL-10 −/− ) mice. To elucidate correlation between...
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Published in: | Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2016-12, Vol.80 (12), p.2318-2324 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | IL-10 is important for stress modulation, and impaired IL-10 function can cause premature mammary gland involution and pup alopecia.
Recently, we found that maternal stress could induce premature mammary gland involution in interleukin 10 knock out (IL-10
−/−
) mice. To elucidate correlation between stress, IL-10, and mammary gland involution, corticosterone was injected into the lactating wild type and IL-10-deficient mice and assessed mammary gland phenotype. Repetitive corticosterone injection developed premature mammary gland involution only in B6.IL-10
−/−
mice; moreover, it induced alopecia in nursing pups. Corticosterone injection induced several typical changes such as mammary gland epithelial cell apoptosis, macrophage infiltration, fat deposition in adipocyte, STAT3 phosphorylation, and upregulation of tyrosine hydroxylase gene in adrenal gland. Overall incidence of pup alopecia and mammary gland involution was relatively high in corticosterone than control B6.IL-10
−/−
group (57% vs. 20%). Our finding demonstrates that IL-10 is important for stress modulation, and B6.Il-10
−/−
with corticosterone has several advantage such as simple to establish, well-defined onset of mammary gland involution, high incidence, and inducing pup alopecia. |
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ISSN: | 0916-8451 1347-6947 |
DOI: | 10.1080/09168451.2016.1214556 |