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In endothelial cell models, BPC-157 significantly enhanced ERK1/2 phosphorylation in a dose-dependent manner, leading to increased cellular proliferation, migration, and vascular tube formation

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have explained a different mechanism of increased barrier permeability, where MMP-9 is implicated in the activation of myosin light chain kinase (MLCK), an enzyme responsible for the phosphorylation of myosin light chain (MLC), a regulator of perijunctional actinomyosin contractility