When human aortic endothelial cells are stacked, specific proteins involved in cellular transport and ribosome function relocate within the cell, and this is linked to higher levels of inflammatory...
Mechanism
Synthesis from 1 study
When endothelial cells stack up, their internal machinery gets scrambled, causing key protein-making parts to move into the nucleus. This switch turns up the production of inflammatory signals, which flood out and trigger artery inflammation. The process is direct: stacking → nuclear shift → more...
Most probable mechanism
When endothelial cells pile up on top of each other, their internal structure gets disrupted, causing parts of their protein-making factory to move into the nucleus. This shift activates the nucleus to produce more building blocks for inflammatory signals, which then get released in large amounts, triggering inflammation in the artery wall.
Physical stacking of endothelial cells disrupts cytoskeletal organization, leading to loss of normal cell shape and internal architecture.
Disrupted cytoskeletal integrity causes the Golgi apparatus and COPII vesicle components to detach from the cytoplasm and translocate into the nucleus.
Nuclear translocation of Golgi and COPII components facilitates the import of ribosomal protein RPL23 into the nucleolus, where it accumulates and alters nucleolar structure.
RPL23 accumulation in the nucleolus enhances ribosomal biogenesis and increases translational capacity for specific mRNAs encoding proinflammatory cytokines.
Elevated translation of IL-6, MCP-1, and CXCL8 mRNAs leads to increased synthesis and secretion of these cytokines into the surrounding tissue.
Evidence from Studies
Supporting (1)
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Stacked human aortic endothelial cells induce atherosclerotic fatty streaks and release proinflammatory cytokines and chemokines
Contradicting (0)
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