| Project/Area Number |
10660291
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Rakuno Gakuen University |
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Principal Investigator |
OKADA Hiroyuki Rakuno Gakuen University, Department of Veterinary Pathology, Associate Professor, 獣医学部, 助教授 (50166419)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | parathyroid hormone-related protein / mammary gland / bovine / paracrine / monensin / cytochalasin B / colchicine / 上皮小体ホルモン関連タンパク / サイトカラシン / 乳腺上皮 |
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| Research Abstract |
Parathyroid hormone-related protein (PTHrP) that had parathyroid hormone-like function and Structure was identified in 1987 as a major factor of humoral hypercalcemia of malignancy. PTHrP is produced in many normal tissues including the lactating mammary gland, however the role of PTHrP is still unclear. Mammary tissues were collected from lactating Holstein dairy cows at 1 week after calving. The mammary tissues were enzymatically digested to release glandular acini. The cells were plated in 24-well collagen-coated plastic culture plates. After confluent at day 6, various concentrations of monensin, colchicine, and cytochalasin B were supplemented to the medium to investigate the change of PTHrP production. The PTHrP production decreased in the cells supplemented with monensin and cytochalasin B in a dose-dependent manner, whereas its production slightly increased by the stimulation with colehicine. Expression of PTHrP mRNA investigated by using reverse transcription-polymerase chain reaction and in situ hybridization techniques decreased when the cells were treated with monensin. This study indicated that PTHrP production from mammary epithelial cells might associated with the formation of actin filaments in the cytoplasm but not with that of microtubules, suggesting that PTHrP might secrete from mammary epithelial cells by the constitutive pathway but not the regulated pathway. Morphologically, mammary epithelial cells treated with monensin were swollen. This finding also suggested that PT1JrP production was inhibited by the inhibition of intracellular vesicle transport.
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