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Bradykinin stimulates prostaglandin E2 release in human skeletal muscular fibroblasts.
Molecular and Cellular Endocrinology ( IF 3.8 ) Pub Date : 2020-02-27 , DOI: 10.1016/j.mce.2020.110771 Antonella Muscella 1 , Luca Giulio Cossa 1 , Carla Vetrugno 1 , Santo Marsigliante 1
Molecular and Cellular Endocrinology ( IF 3.8 ) Pub Date : 2020-02-27 , DOI: 10.1016/j.mce.2020.110771 Antonella Muscella 1 , Luca Giulio Cossa 1 , Carla Vetrugno 1 , Santo Marsigliante 1
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Local mediator prostaglandins and bradykinin are involved in inflammation and pain. We explored bradykinin effects on prostaglandin E2 (PGE2) release from fibroblasts derived from human skeletal muscular biopsies. Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin. Consistently, bradykinin induced both mRNA cyclooxygenase 2 (COX-2) and protein. Bradykinin also induced ERK1/2 and p38 phosphorylation and provoked the translocation from the cytosol to the nucleus of p65/NF-kB. The release of PGE2 by bradykinin could be blocked inhibiting COX-2 and p65/NF-kB, ERK1/2 or p38 activation. Both ERK1/2 and p38 were upstream to NF-kB inasmuch siRNAs significantly blocked the p65/NF-kB activation induced by bradykinin. Thus, bradykinin, acting via B2 receptors, induced PGE2 release through ERK1/2 and p38-dependent pathways and consequent p65/NF-kB translocation to nucleus. p65/NF-kB induced COX-2 transcription. The release of PGE2 provide a possible explanation for the role of bradykinin in inflammatory diseases.
中文翻译：
缓激肽刺激人骨骼肌成纤维细胞中前列腺素E2的释放。
局部介质前列腺素和缓激肽与炎症和疼痛有关。我们探讨了缓激肽对前列腺素E2（PGE2）从人骨骼肌活检组织衍生的成纤维细胞释放的影响。缓激肽通过缓激肽B2受体诱导PGE2释放，因为PGE2释放被缓激肽B2受体选择性拮抗剂FR173657和B2受体激动剂（Hyp3）-缓激肽显示出与缓激肽相当的作用。一致地，缓激肽同时诱导mRNA环氧合酶2（COX-2）和蛋白质。缓激肽还诱导ERK1 / 2和p38磷酸化，并引起从胞质溶胶到p65 / NF-kB核的易位。缓激肽可释放PGE2，从而抑制COX-2和p65 / NF-kB，ERK1 / 2或p38的活化。ERK1 / 2和p38都位于NF-kB的上游，因为siRNA显着阻断了缓激肽诱导的p65 / NF-kB激活。因此，缓激肽通过B2受体起作用，通过ERK1 / 2和p38依赖性途径诱导PGE2释放，进而使p65 / NF-kB易位至细胞核。p65 / NF-kB诱导COX-2转录。PGE 2的释放为缓激肽在炎性疾病中的作用提供了可能的解释。
更新日期：2020-02-27
中文翻译：
缓激肽刺激人骨骼肌成纤维细胞中前列腺素E2的释放。
局部介质前列腺素和缓激肽与炎症和疼痛有关。我们探讨了缓激肽对前列腺素E2（PGE2）从人骨骼肌活检组织衍生的成纤维细胞释放的影响。缓激肽通过缓激肽B2受体诱导PGE2释放，因为PGE2释放被缓激肽B2受体选择性拮抗剂FR173657和B2受体激动剂（Hyp3）-缓激肽显示出与缓激肽相当的作用。一致地，缓激肽同时诱导mRNA环氧合酶2（COX-2）和蛋白质。缓激肽还诱导ERK1 / 2和p38磷酸化，并引起从胞质溶胶到p65 / NF-kB核的易位。缓激肽可释放PGE2，从而抑制COX-2和p65 / NF-kB，ERK1 / 2或p38的活化。ERK1 / 2和p38都位于NF-kB的上游，因为siRNA显着阻断了缓激肽诱导的p65 / NF-kB激活。因此，缓激肽通过B2受体起作用，通过ERK1 / 2和p38依赖性途径诱导PGE2释放，进而使p65 / NF-kB易位至细胞核。p65 / NF-kB诱导COX-2转录。PGE 2的释放为缓激肽在炎性疾病中的作用提供了可能的解释。
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