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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.4
- 수록면
- 102 - 119 (18page)
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초록· 키워드
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We investigated effects of reblastatins on phenotypic changes in monocytes/macrophages induced by 27-hydroxycholesterol (27OHChol). Treatment of THP-1 monocytic cells with reblastatin derivatives, such as 17-demethoxy-reblastatin (17-DR), 18-dehydroxyl-17-demethoxyreblastatin (WK88-1), 18-hydroxyl-17-demethoxyreblastatin (WK88-2), and 18-hydroxyl-17-demethoxy-4,5-dehydroreblastatin (WK88-3), resulted in blockage of CCL2, CCL3, and CCL4 expression at the transcription and protein levels, which, in turn, impaired migration of monocytes/macrophages and Jurkat T cells expressing CCR5, and almost complete inhibition of transcription of M1 marker cytokines, like CXCL10, CXCL11, and TNF-α. Reblastatins also downregulated surface CD14 as well as soluble CD14 along with inhibition of LPS response and matrix metalloprotease-9 expression. Surface levels of mature dendritic cell (mDC)-specific markers, including CD80, CD83, CD88, CD197, and MHC class I and II molecules, were remarkably down-regulated, and 27OHChol-induced decrease of endocytic activity was recovered following treatment with 17-DR, WK88-1, WK88-2, and WK88-3. However, 15-hydroxyl-17-demethoxyreblastatin (DHQ3) did not affect the molecular or functional changes in monocytic cells induced by 27OHChol. Furthermore, surface levels of CD105, CD137, and CD166 were also down-regulated by 17-DR, WK88-1, WK88-2, and WK88-3, but not by DHQ3. Collectively, results of the current study indicate that, except DHQ3, reblastatins regulate the conversion and differentiation of monocytic cells to an immunostimulatory phenotype and mDCs, respectively, which suggests possible applications of reblastatins for immunomodulation in a milieu rich in oxygenated cholesterol molecules.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
참고문헌 (39)
참고문헌 신청
Madrigal-Matute J / 2010 / Heat shock protein 90 inhibitors attenuate inflammatory responses in atherosclerosis / Cardiovasc Res 86:330~337
Mu H / 2017 / HSP90 inhibition suppresses inflammatory response and reduces carotid atherosclerotic plaque formation in ApoE mice / Cardiovasc Ther 35:e12243
Kim J / 2014 / The role of heat shock protein 90 in migration and proliferation of vascular smooth muscle cells in the development of atherosclerosis / J Mol Cell Cardiol 72:157~167
Kim W / 2009 / Rational biosynthetic engineering for optimization of geldanamycin analogues / ChemBioChem 10:1243~1251
Neckers L / 2003 / Heat shock protein 90 / Curr Opin Oncol 15:419~424
Mu H / 2017 / HSP90 inhibition suppresses inflammatory response and reduces carotid atherosclerotic plaque formation in ApoE mice / Cardiovasc Ther 35:e12243
Kim J / 2014 / The role of heat shock protein 90 in migration and proliferation of vascular smooth muscle cells in the development of atherosclerosis / J Mol Cell Cardiol 72:157~167
Kim W / 2009 / Rational biosynthetic engineering for optimization of geldanamycin analogues / ChemBioChem 10:1243~1251
Neckers L / 2003 / Heat shock protein 90 / Curr Opin Oncol 15:419~424
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UCI(KEPA) : I410-ECN-0101-2020-517-000894420