Why the study?
Does whole blood application alter the time course of MLC20 phosphorylation in a rat femoral artery model of vasospasm compared to platelet-rich plasma?
Does whole blood application alter the time course of MLC20 phosphorylation in a rat femoral artery model of vasospasm compared to platelet-rich plasma?
In a rat model of vasospasm, MLC20 phosphorylation mediates early arterial narrowing, whereas later sustained narrowing occurs via MLC20-independent mechanisms.
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Phase-specific MLC20 targeting may warrant exploration in early vasospasm; leaves open independent mechanisms for sustained narrowing in clinical models.
THE PHOSPHORYLATION OF an Mr 20,000 myosin light chain (MLC20) promotes the generation of contractile force through actin-myosin adenosine triphosphatase in most agonist-mediated vascular smooth muscle cell contraction. However, the role of calcium-mediated contractile processes in sustained arterial narrowing after subarachnoid hemorrhage remains unknown. In a femoral artery model of vasospasm, whole blood was applied to arteries in 54 rats for periods of 2 to 10 days; the contralateral artery treated with platelet-rich plasma served as matched control. During the early stage of vasospasm (Days 2–5), in the media of arteries exposed to blood, MLC20 phosphorylation (including diphosphorylated forms) increased significantly (30–38%; P < 0.05); total medial MLC20 during this interval was comparable to that in controls. After 5 days, however, total MLC20 decreased markedly (>90%; P < 0.01) compared with controls; phosphorylated MLC20 was undetectable during this interval. MLC20-mediated contractile processes may be prominent in the early stages of arterial narrowing after subarachnoid hemorrhage; later stages are associated with the loss of MLC20 and the possible persistence of arterial narrowing by other mechanisms.
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Harada et al. (1995) studied this question.
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