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Published on: October 12, 2017
Intermedin inhibits uptake of oxidized LDL via CD36 pathway in RAW264.7 cells
Insights
Intermedin (IMD) prevents atherosclerosis by inhibiting foam cell formation. IMD reduces intracellular cholesterol accumulation and down-regulates CD36 expression, suggesting a CD36-dependent therapeutic mechanism.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiovascular Research
Background:
- Atherosclerosis is a major cardiovascular disease.
- Foam cell formation is a key process in atherosclerosis development.
- The protective mechanism of Intermedin (IMD) against atherosclerosis is not fully understood.
Purpose of the Study:
- To investigate the molecular mechanism of Intermedin (IMD) in preventing foam cell formation.
- To determine the role of CD36 in IMD's protective effects.
Main Methods:
- RAW264.7 cells were used to study foam cell formation.
- Intracellular cholesterol accumulation was measured.
- CD36 expression was analyzed using real-time quantitative reverse transcription-PCR and Western blot.
Main Results:
- Intermedin (IMD) significantly inhibited intracellular cholesterol accumulation in RAW264.7 cells.
- IMD dose-dependently down-regulated CD36 expression.
- The inhibitory effect of IMD on foam cell formation is partly dependent on CD36.
Conclusions:
- Intermedin (IMD) inhibits foam cell formation through a CD36-dependent mechanism.
- IMD shows potential as a therapeutic candidate for treating atherosclerosis.
Abstract:
Intermedin (IMD) exerts a potent function in preventing atherosclerosis, while the mechanism remains unclear. Here we investigated the potential molecular mechanism responsible for the protective function of IMD in preventing foam cell formation in RAW264.7 cells. In our present study, IMD significantly inhibited intracellular cholesterol accumulation. Additionally, IMD dose-dependently down-regulated CD36 expression, which was confirmed by real-time quantitative reverse transcription-PCR and Western blot analysis. Our data suggest that IMD could inhibit the formation of foam cells through, at least partly, a CD36-dependent mechanism. This study suggests that IMD may be a therapeutic candidate for treating atherosclerosis.
