TY - JOUR T1 - Airway smooth muscle myosin phosphatase target subunit 1 phosphorylation in allergic asthma model JF - European Respiratory Journal JO - Eur Respir J VL - 44 IS - Suppl 58 SP - P859 AU - Mayra Álvarez Santos AU - Olivuia Reynoso Ducoing AU - Javier Ambrosio AU - Blanca Bazán Perkins Y1 - 2014/09/01 UR - http://erj.ersjournals.com/content/44/Suppl_58/P859.abstract N2 - Introduction Airway smooth muscle (ASM) contraction has a crucial role in obstruction and hyperresponsiveness (AHR) in asthma. Contraction is produced by the interaction of actin and myosin and relaxation occurs by the activation of myosin light chain phosphatase (MLCP). Activation of MLCP is induced by the phosphorylation of the myosin light chain phosphatasetarget subunit 1 (MYPT1), a regulatory subunit of MLCP, at Ser-507 and Ser-668, and the inhibition by Thr-696 and Thr-853 phosphorylation. It is unknown if MYPT1 is phosphorylated during asthma in vivo. Objective We determinated the phosphorylation patterns of ASM MYPT1 in an asthma model. MethodsSensitized guinea pigs were intermittently challenged with ovalbumin (OA; applied every 10 days). At third OA challenge, the AHR and the expression of MTPY1 in ASM by two dimensional western blot were evaluated. Controls received saline solution instead of OA. Results All sensitized guinea pigs showed airway obstruction after challenges and AHR. ASM in control guinea pigs expresses 3 isoforms of MPTY1 (64, 73 and 194 Da), but only the 73 Da isoform increased its expression in an asthma model. In addition, 73 Da isoform was observed phosphorylated in Ser-507 and Ser-668 in controls and asthma model, although in the latter the expression was higher. MYPT1 was not phosphrorylated in Thr-696 and Thr-853 in controls, but was phosphorylated in asthma model. ConclusionsWe suggest that the inactivation of MYPT1 by phosphorylation of Thr-969 and Thr-853 contributes to AHR development in an asthma model in vivo. ER -