1997
DOI: 10.1161/01.cir.96.12.4357
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Enhanced Myosin Light Chain Phosphorylations as a Central Mechanism for Coronary Artery Spasm in a Swine Model With Interleukin-1β

Abstract: These results indicate that enhanced MLC phosphorylations in the vascular smooth muscle play a central role in the pathogenesis of coronary spasm in our swine model.

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Cited by 140 publications
(109 citation statements)
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“…10 Fasudil and hydroxyfasudil are cell-permeable and potently inhibit Rho-kinase and MLC phosphorylation in vascular smooth muscle cells. 14,22 The phosphorylation of MLC is required for its interaction with actin filaments, forming actin stress fibers and focal adhesion complexes. Indeed, inhibition of Rho-kinase by hydroxyfasudil enhances cerebral blood flow 23 and prevents cerebral vasospasm after subarachnoid hemorrhage.…”
Section: Discussionmentioning
confidence: 99%
“…10 Fasudil and hydroxyfasudil are cell-permeable and potently inhibit Rho-kinase and MLC phosphorylation in vascular smooth muscle cells. 14,22 The phosphorylation of MLC is required for its interaction with actin filaments, forming actin stress fibers and focal adhesion complexes. Indeed, inhibition of Rho-kinase by hydroxyfasudil enhances cerebral blood flow 23 and prevents cerebral vasospasm after subarachnoid hemorrhage.…”
Section: Discussionmentioning
confidence: 99%
“…For example, the activation of Cdc42 induces actin-rich surface protrusions, whereas activation of Rac1 leads to the formation of lamellipodia and membrane ruffles. By contrast, the activation of Rho and its downstream target, Rho-associated protein kinase (ROCK), regulates calcium-insensitive vascular smooth-muscle contraction in hypertension [39] and coronary spasm [40]. Because three-dimensional colocalization of intracellular proteins is regulated by cytoskeletal rearrangements, changes in statin-induced actin cytoskeleton could affect intracellular transport, membrane trafficking, mRNA stability and gene transcription.…”
Section: Other Small Gtpasesmentioning
confidence: 99%
“…23 We have previously demonstrated that fasudil/ hydroxyfasudil suppresses myosin light chain phosphorylation. 5,6,24 Mutation of the cardiac myosin regulatory light chain near the phosphorylation site causes significant cardiac hypertrophy in humans. 25 These results suggest that Rho-kinase activation is involved in the pathogenesis of LV remodeling.…”
Section: Remodeling and Rho-kinasementioning
confidence: 99%