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首页> 外文期刊>Biology Open >Effect of okadaic acid on cultured clam heart cells: involvement of MAPkinase pathways
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Effect of okadaic acid on cultured clam heart cells: involvement of MAPkinase pathways

机译：冈田酸对蛤lam心脏细胞的影响：MAP激酶途径的参与

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Okadaic acid (OA) is one of the main diarrhetic shellfish poisoning toxins and a potent inhibitor of protein phosphatases 1 and 2A. The downstream signal transduction pathways following the protein phosphatase inhibition are still unknown and the results of most of the previous studies are often conflicting. The aim of the present study was to evaluate the effects of OA on heart clam cells and to analyse its possible mechanisms of action by investigating the signal transduction pathways involved in OA cytotoxicity. We showed that OA at 1?μM after 24?h of treatment induces disorganization of the actin cytoskeleton, rounding and detachment of fibroblastic cells. Moreover, treatment of heart cells revealed a sequential activation of MAPK proteins depending on the OA concentration. We suggest that the duration of p38 and JNK activation is a critical factor in determining cell apoptosis in clam cardiomyocytes. In the opposite, ERK activation could be involved in cell survival. The cell death induced by OA is a MAPK modulated pathway, mediated by caspase 3-dependent mechanism. OA was found to induce no significant effect on spontaneous beating rate or inward L-type calcium current in clam cardiomyocytes, suggesting that PP1 was not inhibited even by the highest dose of OA.
机译：冈田酸（OA）是主要的腹泻性贝类中毒毒素之一，是蛋白质磷酸酶1和2A的有效抑制剂。蛋白磷酸酶抑制后的下游信号转导途径仍是未知的，并且大多数先前研究的结果常常是矛盾的。本研究的目的是通过研究涉及OA细胞毒性的信号转导途径来评估OA对心脏蛤lam细胞的作用并分析其可能的作用机制。我们显示，在治疗24小时后，以1？μM的OA诱导肌动蛋白细胞骨架的紊乱，成纤维细胞的舍入和脱离。此外，对心脏细胞的治疗揭示了取决于OA浓度的MAPK蛋白的顺序激活。我们建议p38和JNK激活的持续时间是决定蛤心肌细胞凋亡的关键因素。相反，ERK激活可能与细胞存活有关。 OA诱导的细胞死亡是MAPK调节的途径，由caspase 3依赖性机制介导。发现OA对蛤类心肌细胞的自发搏动率或内向L型钙电流没有明显影响，这表明即使最大剂量的OA也不能抑制PP1。

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