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NOS1-derived nitric oxide facilitates macrophage uptake of low-density lipoprotein.
Date
2019-02-25
Author
Roy, A
Banerjee, Sreeparna
Saqib, U
Baig, MS
Metadata
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Foam cell formation is a hallmark event during atherosclerosis. The current paradigm is that lipid uptake by a scavenger receptor in macrophages initiates necrosis core formation that characterizes atherosclerosis. We report that NOS1‐derived nitric oxide (NO) facilitates low‐density lipoprotein (LDL) uptake by macrophages independent of the inflammatory response. LDL uptake could be dramatically suppressed by NOS1 specific inhibitor 1‐(2‐trifluoromethylphenyl) imidazole (TRIM). Importantly, the notion that NOS1 can mediate uptake of lipoproteins suggests that the foam cell formation is regulated by NOS1‐derived NO‐mediated mechanism. This is a novel study involving NOS1 as a critical player of foam cell formation and reveals much about the key molecular proteins involved in atherosclerosis. Targeting NOS1 would be a useful strategy in reducing LDL uptake by macrophages and hence dampening the atherosclerosis progression.
Subject Keywords
Cell Biology
,
Biochemistry
,
Molecular Biology
URI
https://hdl.handle.net/11511/38732
Journal
Journal of cellular biochemistry
DOI
https://doi.org/10.1002/jcb.28439
Collections
Department of Biology, Article
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A. Roy, S. Banerjee, U. Saqib, and M. Baig, “NOS1-derived nitric oxide facilitates macrophage uptake of low-density lipoprotein.,”
Journal of cellular biochemistry
, 2019, Accessed: 00, 2020. [Online]. Available: https://hdl.handle.net/11511/38732.