| Project/Area Number |
18591264
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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 |
Dermatology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
OKAMOTO Hiroyuki Kansai Medical University, Dermatology, Associate Professor (10142291)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUNO Kana Kansai Medical University, Dermatology, Instructor (90351543)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,750,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥450,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Sarcoidosis / Granuloma / ACE / Monocytes / Angiotensin-II / アンギオーテンシンII / アンギオテンシンII |
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| Research Abstract |
We investigated whether expression of ACE on monocytes is augmented in the process of differentiation into multinucleated giant cells and the production of Ang-II is enhanced. Multinucleated giant cells showed higher expression of ACE than freshly isolated monocytes, cultured monocytes and monocytes stimulated by ConA. However the higher mRNAlevel of ACE could not confirm by RTPCR method Because activity of ACE level in the supernatant of cultured cells was faint, no difference in culture condition was detected. ACE in the cytoplasm of monocytes was not detected by fluorometric assay. Ang-II levels were increased in the supernatant of cultured monocytes. This increment was inhibited by addition of captril, an inhibitor of ACE. The expression of ACE was inhibited by calphostinC, wortmannin, UO126, and PP2. The expression was also inhibited by tranilast and aloprinol.
When freshly isolated monocytes were cultured in the presence of M-CSF/IL-10 or TGF-β/IL-10, CD14^+CD16^+ monocytes were induced. On the other hand, when Ang-II was added, the induction was inhibited Locomotion ability of Ang-II-stimulated monocytes was decreased against monceyte chemoattractant protein-1.
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