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| Research article summary (published 17 May 2006): |
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Expression of calcitonin receptor in rat mammary gland during lactation.
Full Abstract
Calcitonin (CT) and calcitonin receptor (CTR) have been reported to play an important role in mammary tissue during pregnancy, lactation, and involution. In the present study, the expression and distribution of CTR mRNA in rat mammary tissue during pregnancy and lactation were investigated. As measured by real-time RT-PCR, CTR mRNA levels were increased only slightly during pregnancy, but increased markedly immediately postpartum and remained elevated through lactation, with the highest levels observed 14 days postpartum. In situ hybridization analysis showed that intense CTR mRNA signals were detected in the whole mammary gland. We performed immunohistochemistry to determine distribution of CTR in the mammary epithelium. CTR has been reported to act as an amylin receptor when heterodimerized with receptor activity modifying protein-1 (RAMP1) or RAMP3. mRNA expression of RAMP1 and RAMP3 in mammary tissue decreased during pregnancy and lactation, and amylin mRNA was undetectable, suggesting that up-regulated CTR in lactating mammary tissues binds CT rather than amylin. In primary cultures of mammary cells isolated from rat dams 14 days postpartum, CT produced a statistically significant decrease in thymidine incorporation. These results suggest that up-regulation of CTR during lactation may contribute to inhibition of mammary epithelial cell proliferation.
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Author information
Author/s: Ishii, Aiko (A); Nakamura, Misa (M); Nakamura, Atsushi (A); Takeda, Koichi (K); Han, Bo (B); Kakudo, Kennichi (K);
Affiliation: Department of Pathology, Wakayama Medical University, Wakayama, Japan.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Endocrine journal (Endocr J), published in Japan. (Language: eng)
Reference: 2006-Jun; vol 53 (issue 3) : pp 317-24
Dates: Created 2006/06/27; Completed 2006/10/20; Revised 2006/11/15;
PMID: 16710074, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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