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USP22 activates apoptotic cell clearance. 14 / 14
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"USP22 enhances atherosclerotic plaque stability and macrophage efferocytosis by stabilizing PPARgamma."
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"We unexpectedly found that USP22 in macrophages enhanced efferocytosis both in vitro and in vivo."
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"In this study, we likewise found that silencing USP22 promotes the uptake of oxidized lipoproteins, which may inhibit macrophage efferocytosis.Interestingly, in this study, we found that USP22 promoted the expression of efferocytosis-associated receptors as well as bridging molecules and that this regulation is dependent on the activation of PPARγ."
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"In addition, to determine the mechanism by which silencing USP22 inhibits efferocytosis, we used CytD to inhibit actin polymerization in THP-1-derived macrophages, which prevented the internalization of ACs."
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"We subsequently used adeno-associated virus overexpressing USP22 in macrophages to investigate its biological properties and found that USP22 could promote efferocytosis and stabilize plaques by regulating PPARγ."
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"We next investigated whether USP22 enhances efferocytosis by regulating PPARγ."
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"Finally, we tested whether the decrease in PPARγ might be one of the molecular mechanisms by which USP22 silencing inhibits efferocytosis."
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"Our results showed that the PPARγ agonist rosiglitazone reversed the decrease in macrophage efferocytosis caused by USP22 silencing (Fig. 5H–J, Supplementary Fig. S5A, B. Furthermore, for THP-1-derived macrophages under inflammatory conditions, USP22 overexpression also promoted efferocytosis."
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"In addition, we cannot completely exclude the possible role of USP22 in other cell types in atherosclerosis in this study.In conclusion, we showed that USP22 in macrophages promotes efferocytosis and alleviates the progression of atherosclerosis in ApoE mice by regulating PPARγ."
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"We subsequently determined whether GW9662 influenced the promotion of efferocytosis by USP22 overexpression in macrophages in vivo."
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"The results revealed that the ratio of macrophage-associated TUNEL-positive cells to free TUNEL-positive cells was greater in the lesions of ApoE mice with USP22 overexpression in macrophages than in those of controls (Fig. 2F), which indicated that USP22 enhanced efferocytosis, and these results were consistent with the smaller necrotic core area found in the aortas of ApoE mice with USP22 overexpression in macrophages (Fig. 2C)."
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"USP22 in macrophages enhances efferocytosis."
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"We observed in vivo that overexpression of USP22 in macrophages enhanced efferocytosis."
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"We performed GSEA on the differential expression of transcripts (Supplementary data 1), which suggested that USP22 may promote efferocytosis (Supplementary Fig. S3C)."
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