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首页> 外文期刊>The European Journal of Neuroscience >Cysteinyl-leukotrienes are released from astrocytes and increase astrocyte proliferation and glial fibrillary acidic protein via cys-LT receptors and mitogen-activated protein kinase pathway.
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Cysteinyl-leukotrienes are released from astrocytes and increase astrocyte proliferation and glial fibrillary acidic protein via cys-LT receptors and mitogen-activated protein kinase pathway.

机译：半胱氨酰白三烯从星形胶质细胞中释放出来，并通过cys-LT受体和有丝分裂原激活的蛋白激酶途径增加星形胶质细胞的增殖和神经胶质原纤维酸性蛋白。

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Abstract Cysteinyl-leukotrienes (cys-LTs), potent mediators in inflammatory diseases, are produced by nervous tissue, but their cellular source and role in the brain are not very well known. In this report we have demonstrated that rat cultured astrocytes express the enzymes (5'-lipoxygenase and LTC(4) synthase) required for cys-LT production, and release cys-LTs in resting condition and, to a greater extent, in response to calcium ionophore A23187, 1 h combined oxygen-glucose deprivation or 2-methyl-thioATP, a selective P2Y(1)/ATP receptor agonist. MK-886, a LT synthesis inhibitor, prevented basal and evoked cys-LT release. In addition, 2-methyl-thioATP-induced cys-LT release was abolished by suramin, a P2 receptor antagonist, or by inhibitors of ATP binding cassette proteins involved in cys-LT release. We also showed that astrocytes express cys-LT(1) and not cys-LT(2) receptors. The stimulation of these receptors by LTD(4) activated the mitogen-activated protein kinase (MAPK) pathway. This effect was: (i) insensitive to inhibitors of receptor-coupled Gi protein (pertussis toxin) or tyrosine kinase receptors (genistein); (ii) abolished by MK-571, a cys-LT(1) selective receptor antagonist, or PD98059, a MAPK inhibitor; (iii) reduced by inhibitors of calcium/calmodulin-dependent kinase II (KN-93), Ca(2+)-dependent and -independent (GF102903X) or Ca(2+)-dependent (Go6976) protein kinase C isoforms. LTD(4) also increased astrocyte proliferation and glial fibrillary acidic protein content, which are considered hallmarks of reactive astrogliosis. Both effects were counteracted by cell pretreatment with MK-571 or PD98059. Thus, cys-LTs released from astrocytes might play an autocrine role in the induction of reactive astrogliosis that, in brain injuries, contributes to the formation of a reparative glial scar.
机译：摘要半胱氨酸-白三烯（cys-LTs）是炎症性疾病的有效介体，由神经组织产生，但它们的细胞来源和在脑中的作用还不是很清楚。在本报告中，我们证明了大鼠培养的星形胶质细胞表达产生cys-LT所需的酶（5'-脂加氧酶和LTC（4）合酶），并在静止状态下释放cys-LTs，并且在更大程度上响应于钙离子载体A23187，1小时结合氧-葡萄糖剥夺或2-甲基-硫代ATP，选择性P2Y（1）/ ATP受体激动剂。 LT合成抑制剂MK-886可阻止基础和诱发的cys-LT释放。另外，P2受体拮抗剂苏拉明或与cys-LT释放有关的ATP结合盒蛋白的抑制剂消除了2-甲基-硫代ATP诱导的cys-LT释放。我们还显示星形胶质细胞表达cys-LT（1）而不是cys-LT（2）受体。 LTD（4）对这些受体的刺激激活了有丝分裂原激活的蛋白激酶（MAPK）途径。这种作用是：（i）对受体偶联的Gi蛋白（百日咳毒素）或酪氨酸激酶受体（染料木黄酮）的抑制剂不敏感; （ii）被cys-LT（1）选择性受体拮抗剂MK-571或MAPK抑制剂PD98059废除; （iii）通过钙/钙调蛋白依赖性激酶II（KN-93），Ca（2+）依赖性和非依赖性（GF102903X）或Ca（2+）依赖性（Go6976）蛋白激酶C亚型的抑制剂降低。 LTD（4）还增加了星形胶质细胞增殖和神经胶质纤维酸性蛋白含量，这被认为是反应性星形胶质增生的标志。两种作用都可以通过用MK-571或PD98059进行细胞预处理来抵消。因此，从星形胶质细胞释放的cys-LTs可能在诱导反应性星形胶质增生中起自分泌作用，后者在脑损伤中有助于形成修复性神经胶质瘢痕。

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