Key result
AYPGKF and thrombin activate Src and p38-MAPK pathways via PAR-4 in cardiomyocytes, distinct from PAR-1.
Population
Cardiomyocytes, including those cultured from PAR-1(-/-) mice and PAR-1(-/-) cells stably overexpressing PAR-4
Comparison
PAR-4 activation using AYPGKF or thrombin vs PAR-1 activation (SFLLRN)
Design
Preclinical
Authors
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May inform PAR-4 targeting in cardiac inflammation; leaves open relevance to human remodeling.
PAR-4 exhibits a unique signaling phenotype in cardiomyocytes involving Src and EGFR transactivation, which may influence cardiac remodeling during inflammation.
Sabri et al. (2003) studied this question. AYPGKF and thrombin vs. SFLLRN (PAR-1 agonist) was evaluated on Src and p38-MAPK activation, EGFR/ErbB2 transactivation. AYPGKF and thrombin activate Src and the p38-MAPK signaling pathway via PAR-4 in cardiomyocytes, identifying a unique signaling phenotype distinct from PAR-1.
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