Key result
Very low-density lipoprotein (VLDL) and dietary triglycerides directly regulate gene expression in macrophages via the activation of peroxisome proliferator-activated receptor delta.
This study identifies a novel pathway where dietary triglycerides and VLDL directly regulate gene expression in macrophages via PPARδ, providing a molecular basis for lipoprotein-driven atherogenesis.
May link dietary triglycerides to macrophage inflammation; leaves open human relevance and clinical translation.
Although triglyceride-rich particles, such as very low-density lipoprotein (VLDL), contribute significantly to human atherogenesis, the molecular basis for lipoprotein-driven pathogenicity is poorly understood. We demonstrate that in macrophages, VLDL functions as a transcriptional regulator via the activation of the nuclear receptor peroxisome proliferator-activated receptor delta. The signaling components of native VLDL are its triglycerides, whose activity is enhanced by lipoprotein lipase. Generation of peroxisome proliferator-activated receptor delta null macrophages verifies the absolute requirement of this transcription factor in mediating the VLDL response. Thus, our data reveal a pathway through which dietary triglycerides and VLDL can directly regulate gene expression in atherosclerotic lesions.
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Chawla et al. (2003) studied Atherogenesis. Very low-density lipoprotein (VLDL) was evaluated on Macrophage gene expression. Very low-density lipoprotein (VLDL) and dietary triglycerides directly regulate gene expression in macrophages via the activation of peroxisome proliferator-activated receptor delta.
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