Evaluation of changes of apelin and apelin receptor (APJ) expression in cervix-uterus and placental axis in an LPS-induced preterm labor model.

Sema Avci, Ezgi Golal, Nuray Acar
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Abstract

Although preterm birth is among the preventable causes of maternal and infant death, its mechanism has not yet been clarified. When evaluated in terms of the results, the psycho-social burden of mother-infant losses and the costs of rehabilitation, care, and treatment for postpartum sequelae are high. When evaluated in terms of its causes, infection/inflammation has an important place. Therefore, it is essential to understand the role of pro- and anti-inflammatory proteins in the process. In our study, apelin and apelin receptor (APJ) expression in the cervix-uterus and placental axis were evaluated at tissue and protein levels in pregnant and non-pregnant control, sham, PBS, and LPS groups in the infection model in which LPS induction was performed by midline laparotomy, in CD-1 mice. The evaluation of this axis regarding apelin and apelin receptor in the preterm birth model is new in the literature. Apelin is expressed more intensely in uterine epithelial cells than in the cervix. In the placenta, expression is more intense in the junctional zone compared to other zones. Apelin protein levels decrease significantly in the cervix and placenta whereas it increases in the uterus. While no change was observed in the expression of the apelin receptor at the tissue and protein level in the cervix and uterus, it increased in both aspects in the placenta in the invasive procedure groups. We propose that the decrease in apelin protein due to LPS in the preterm delivery model may be related to the effort to compensate for the balance deteriorated in the pro-inflammatory direction with post-transitional modification at the tissue level. The tendency of apelin to increase with pregnancy has led to the conclusion that it is necessary for a healthy pregnancy. Although the apelin receptor does not change with inflammation, it is necessary to investigate the mechanisms associated with its stress and trauma-induced increase, since it increases in the invasive procedure group.

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评估LPS诱导早产模型中子宫颈和胎盘轴中apelin和apelin受体(APJ)表达的变化。
尽管早产是可预防的母婴死亡原因之一,但其机制尚未阐明。当根据结果进行评估时,母婴损失的心理社会负担以及产后后遗症的康复、护理和治疗费用都很高。当根据其原因进行评估时,感染/炎症具有重要地位。因此,了解促炎和抗炎蛋白在这一过程中的作用至关重要。在我们的研究中,在CD-1小鼠的感染模型中,在组织和蛋白质水平上评估了妊娠和非妊娠对照组、假手术组、PBS组和LPS组中子宫颈、子宫颈和胎盘轴中apelin和apelin受体(APJ)的表达,在感染模型中通过中线剖腹术进行LPS诱导。关于早产模型中apelin和apelin受体的这一轴的评估在文献中是新的。Apelin在子宫上皮细胞中的表达比在宫颈中更强烈。在胎盘中,与其他区域相比,交界区的表达更强烈。Apelin蛋白水平在子宫颈和胎盘中显著降低,而在子宫中则增加。虽然在宫颈和子宫的组织和蛋白质水平上没有观察到apelin受体的表达变化,但在侵入性手术组的胎盘中,它在这两个方面都增加了。我们提出,在早产模型中,LPS导致的apelin蛋白的减少可能与在组织水平上通过过渡后修饰来补偿促炎方向上恶化的平衡有关。apelin随妊娠期增加的趋势导致了一个结论,即它对健康妊娠是必要的。尽管apelin受体不会随着炎症而改变,但有必要研究其应激和创伤诱导的增加的机制,因为它在侵入性手术组中增加。
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