首页> 美国卫生研究院文献>The Journal of Reproduction and Development >Expression of C–C motif chemokines and their receptors in bovine placentomes at spontaneous and induced parturition
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Expression of C–C motif chemokines and their receptors in bovine placentomes at spontaneous and induced parturition

机译:C–C基序趋化因子及其受体在自然分娩和诱发分娩时在胎盘素中的表达

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摘要

In bovine placentomes, the inflammatory response is considered important for the detachment of the fetal membrane from the caruncle after parturition. Glucocorticoids, a trigger of theonset of parturition, facilitate functional maturation of placentomes via prostaglandin (PG) and estrogen production in cattle. This study investigated how exogeneous glucocorticoids, whichexert immunosuppressive effects, affect placental inflammation at parturition. Placentomes were collected immediately after spontaneous or induced parturition. Parturition was conventionallyinduced using PGF2α or dexamethasone or with a combination of triamcinolone acetonide and high-dose betamethasone (TABET treatment). Polymerase chain reaction (PCR) array analysis indicatedthat 9/13 C–C motif chemokine ligands ( ) were upregulated > two-fold in spontaneous parturition, with and being highlyexpressed. The expressions of , C–C motif chemokine receptor 1 ( ), and in caruncles were significantlyhigher in spontaneous parturition than in induced parturition. Although the clinical dose of dexamethasone did not influence the expression of these s and s, TABET treatment increased expression. CCL8, CCR1, CCR2, and CCR5 were localized in the caruncular epithelial cells. CCR2 was also localized inthe epithelial cells of the cotyledonary villi. This study is the first report to reveal the disruption in and expression in bovine placentomes atinduced parturition. Enhanced glucocorticoid exposure for the induction of parturition may upregulate expression in placentomes, but the treatment does not adequatelypromote expression. Additionally, immunohistochemistry suggested that the CCL–CCR system is involved in the functional regulation of maternal and fetal epithelial cellsin placentomes at parturition.
机译:在牛胎盘素中,炎症反应被认为对于分娩后胎膜从颈动脉脱离很重要。糖皮质激素,触发分娩的发生,通过前列腺素(PG)促进胎盘的功能成熟和牛体内雌激素的产生。这项研究调查了外源性糖皮质激素如何发挥免疫抑制作用,影响分娩时的胎盘炎症。自然分娩或诱导分娩后立即收集胎盘。分娩通常是使用PGF2α或地塞米松或曲安奈德和大剂量倍他米松的联合诱导(TABET处理)。指示聚合酶链反应(PCR)阵列分析9/13 C–C基序趋化因子配体()在自发性分娩中被上调>两倍,且高度表达。 ,C–C基序趋化因子受体1()和在甲虫中的表达显着自发性分娩比诱导性分娩更高。尽管地塞米松的临床剂量并不影响这些药物的表达。 s,TABET治疗增加表达。 CCL8,CCR1,CCR2和CCR5定位在肾小管上皮细胞中。 CCR2也位于子叶绒毛的上皮细胞。这项研究是第一个揭示牛胎盘素在胎盘中的破坏和表达的报告。诱发分娩。增强的糖皮质激素暴露以诱导分娩可能会上调胎盘的表达,但治疗效果不佳促进表达。此外,免疫组织化学表明,CCL–CCR系统参与母体和胎儿上皮细胞的功能调节。在胎盘上分娩。

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