ATF3 Inhibits Tenascin-C-induced Foam Cell Formation in LPS-Stimulated THP-1 Macrophages by Suppressing TLR-4
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- Luo Hong
- Key Disciplines Laboratory Clinical-Medicine Henan, Department of Cardiovascular Surgery, the First Affiliated Hospital of Zhengzhou University
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- Wang Jing
- Key Disciplines Laboratory Clinical-Medicine Henan, Department of Stomatology, the First Affiliated Hospital of Zhengzhou University
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- Qiao Chenhui
- Key Disciplines Laboratory Clinical-Medicine Henan, Department of Cardiovascular Surgery, the First Affiliated Hospital of Zhengzhou University
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- Zhang Xin
- Key Disciplines Laboratory Clinical-Medicine Henan, Department of Cardiovascular Surgery, the First Affiliated Hospital of Zhengzhou University
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- Zhang Weihua
- Key Disciplines Laboratory Clinical-Medicine Henan, Department of Cardiovascular Surgery, the First Affiliated Hospital of Zhengzhou University
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- Ma Ning
- Key Disciplines Laboratory Clinical-Medicine Henan, Department of Cardiovascular Surgery, the First Affiliated Hospital of Zhengzhou University
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Aim: Efficiently inhibiting the formation of macrophage foam cells is indispensable for mitigating and treating atherosclerosis. Tenascin-C (TN-C) plays an important role in promoting atherosclerosis; therefore, it is essential to inhibit foam cell formation associated with TN-C for controlling atherosclerosis. Activating transcription factor 3 (ATF3) is one of the factors involved in regulating the complex process of foam cell formation. This study aimed to explore the role of TN-C and ATF3 in LPS-stimulated THP-1-derived macrophages.<br>Methods: RT-PCR was used for evaluating the expression of TN-C in LPS-stimulated THP-1 macrophages. Further, exogenous TN-C was introduced and incubated with cultured THP-1 macrophages to confirm the effect of TN-C on LPS-stimulated THP-1 macrophages. ATF3-modified THP-1 macrophages were constructed and verified by western blot. High performance liquid chromatography (HPLC) assay and Oil red O staining were applied for detecting cholesteryl ester/total cholesterol (CE/TC) and lipid formation in THP-1 macrophages.<br>Results: The expression of TN-C was determined to be upregulated in LPS-stimulated THP-1 macrophages in a dose- and time-dependent manner. HPLC assay and Oil red O staining confirmed that TN-C can enhance LPS-induced THP-1 macrophage foam cell formation. Moreover, ATF3 can act as a negative regulatory factor for inhibiting TN-C-induced foam cell formation by suppressing TLR-4 in LPS-stimulated THP-1 macrophages.<br>Conclusion: ATF3 can inhibit TN-C-induced foam cell formation in LPS-stimulated THP-1 macrophages by suppressing TLR-4. It may be a useful molecular target to control TN-C-induced foam cell formation in atherosclerosis.
収録刊行物
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- Ｊｏｕｒｎａｌ ｏｆ Ａｔｈｅｒｏｓｃｌｅｒｏｓｉｓ ａｎｄ Ｔｈｒｏｍｂｏｓｉｓ
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Ｊｏｕｒｎａｌ ｏｆ Ａｔｈｅｒｏｓｃｌｅｒｏｓｉｓ ａｎｄ Ｔｈｒｏｍｂｏｓｉｓ 22 (11), 1214-1223, 2015
一般社団法人 日本動脈硬化学会