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• W2105496404 abstract "Atherosclerotic plaque develops at sites of disturbed flow. We previously showed that flow activates endothelial cell integrins, which then bind to the subendothelial extracellular matrix (ECM), and, in cells on fibronectin or fibrinogen, trigger nuclear factor-κB activation. Additionally, fibronectin and fibrinogen are deposited into the subendothelial ECM at atherosclerosis-prone sites at early times. We now show that flow activates ECM-specific signals that establish patterns of integrin dominance. Flow induced α2β1 activation in cells on collagen, but not on fibronectin or fibrinogen. Conversely, α5β1 and αvβ3 are activated on fibronectin and fibrinogen, but not collagen. Failure of these integrins to be activated on nonpermissive ECM is because of active suppression by the integrins that are ligated. Protein kinase A is activated specifically on collagen and suppresses flow-induced αvβ3 activation. Alternatively, protein kinase Cα is activated on fibronectin and mediates α2β1 suppression. Thus, integrins actively cross-inhibit through specific kinase pathways. These mechanisms may determine cellular responses to complex extracellular matrices." @default.
• W2105496404 created "2016-06-24" @default.
• W2105496404 creator A5014276750 @default.
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• W2105496404 date "2006-11-01" @default.
• W2105496404 modified "2023-09-30" @default.
• W2105496404 title "Matrix-specific Suppression of Integrin Activation in Shear Stress Signaling" @default.
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• W2105496404 doi "https://doi.org/10.1091/mbc.e06-04-0289" @default.
• W2105496404 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1635406" @default.
• W2105496404 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16928957" @default.
• W2105496404 hasPublicationYear "2006" @default.
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