Xiaofei Liang1,2, Haipeng Guo3,4, Lijuan Shen5, Guangrui Bai3,4, Lina Zhu3,4. 1. Department of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161000, China. liangxiaofeidoctor@163.com. 2. Department of Laboratory Medicine, Affiliated Qiqihar Hospital, Southern Medical University, Qiqihar, 161000, China. liangxiaofeidoctor@163.com. 3. Department of Laboratory Medicine, The First Hospital of Qiqihar, Qiqihar, 161000, China. 4. Department of Laboratory Medicine, Affiliated Qiqihar Hospital, Southern Medical University, Qiqihar, 161000, China. 5. Department of Laboratory Medicine, Qiqihar MingZhu Hospital, Qiqihar, 161000, China.
Abstract
OBJECTIVE: In addition to diet and metabolism, the occurrence of foam cells and atherosclerosis are also related to environmental factors. Individual studies have shown that ultraviolet B (UVB) can regulate the progression of atherosclerosis, but with different results. Whether or not UVB has a dual effect on atherosclerosis and what mechanism is involved has not been reported. METHODS: After THP-1-derived foam cells were treated with UVB in different ways, the effects of UVB on foam cells were investigated by western blotting, cholesterol efflux experiment, oil red O staining and other methods. RESULTS: UVB plays a dual role on foam cell formation, and this effect is related to cholesterol efflux. UVB of 50 mJ/cm2 can promote cholesterol efflux in foam cells, while UVB of 200 mJ/cm2 can inhibit cholesterol efflux. UVB induces cholesterol efflux from foam cells in an autophagy-dependent manner, as the beneficial effect of UVB at 50 mJ/cm2 can be reversed by the autophagy inhibitor 3-Methyladenine (3-MA). In addition, silencing the expression of ultraviolet radiation resistance-associated gene (UVRAG) can inhibit autophagy and reduce cholesterol efflux, and overexpressing UVRAG yields the opposite result. CONCLUSION: In conclusion, our research proves that UVB exhibits a dual role in foam cell formation by regulating cholesterol efflux. Further more, we also reveal that UVRAG-mediated autophagy is the underlying mechanism of UVB-induced cholesterol efflux.
OBJECTIVE: In addition to diet and metabolism, the occurrence of foam cells and atherosclerosis are also related to environmental factors. Individual studies have shown that ultraviolet B (UVB) can regulate the progression of atherosclerosis, but with different results. Whether or not UVB has a dual effect on atherosclerosis and what mechanism is involved has not been reported. METHODS: After THP-1-derived foam cells were treated with UVB in different ways, the effects of UVB on foam cells were investigated by western blotting, cholesterol efflux experiment, oil red O staining and other methods. RESULTS: UVB plays a dual role on foam cell formation, and this effect is related to cholesterol efflux. UVB of 50 mJ/cm2 can promote cholesterol efflux in foam cells, while UVB of 200 mJ/cm2 can inhibit cholesterol efflux. UVB induces cholesterol efflux from foam cells in an autophagy-dependent manner, as the beneficial effect of UVB at 50 mJ/cm2 can be reversed by the autophagy inhibitor 3-Methyladenine (3-MA). In addition, silencing the expression of ultraviolet radiation resistance-associated gene (UVRAG) can inhibit autophagy and reduce cholesterol efflux, and overexpressing UVRAG yields the opposite result. CONCLUSION: In conclusion, our research proves that UVB exhibits a dual role in foam cell formation by regulating cholesterol efflux. Further more, we also reveal that UVRAG-mediated autophagy is the underlying mechanism of UVB-induced cholesterol efflux.