子宫收缩乏力是产后出血的主要原因。我们先前提出了产后急性肌层炎(PAM)的新组织学概念,以阐明子宫收缩乏力的病理生理学。这个概念涉及巨噬细胞和中性粒细胞的浸润,以及子宫肌层中的肥大细胞和补体激活。然而,PAM背景下子宫收缩乏力的病理机制尚不清楚.在这里,我们关注子宫收缩相关蛋白(CAPs),包括连接蛋白43(Cx43),催产素受体(OXR),前列腺素受体EP1,EP3,FP,和蛋白酶激活受体(PAR)-1。这项后续研究旨在比较PAM和对照组之间的CAP表达。我们从2011年至2018年羊水栓塞登记的病例中选择了38名PAM受试者。在剖宫产期间收集10例产妇的对照组织。我们用以下CAP标记对子宫肌层组织进行染色,炎症细胞标志物,和其他标记:Cx43,OXR,EP1,EP3,FP,PAR-1,C5a受体,胰蛋白酶,中性粒细胞弹性蛋白酶,CD68,β-肌动蛋白,和Na+/K+-ATP酶。Cx43,OXR的免疫染色阳性区域,PAM组织中β-肌动蛋白标准化的EP1、EP3和FP明显小于对照组,而PAM组中PAR-1和Na/K-ATPase的含量显着增加。Cx43和OXR阳性区域与CD68和类胰蛋白酶的免疫染色阳性细胞数呈负相关,分别。PAM可能损害个体和同步的心肌细胞收缩,导致子宫收缩难以治疗的子宫收缩。需要进一步的基于细胞的研究来阐明炎症细胞抑制CAP表达的分子机制。
Uterine atony is a major contributor to postpartum hemorrhage. We previously proposed the novel histological concept of postpartum acute myometritis (PAM) to elucidate the pathophysiology of uterine atony. This concept involves the infiltration of macrophages and neutrophils, as well as mast cell and complement activation in the myometrium. However, the pathological mechanism underlying uterine atony in the context of PAM remains unclear. Herein, we focused on uterine contraction-associated proteins (CAPs) including connexin 43 (Cx43), oxytocin receptors (OXR), prostaglandin receptors EP1, EP3, FP, and protease-activated receptor (PAR)-1. This follow-up study aimed to compare CAP expression between PAM and control groups. We selected 38 PAM subjects from the cases enrolled in our amniotic fluid embolism registry between 2011 and 2018. Control tissues from 10 parturients were collected during cesarean section. We stained the myometrial tissues with the following CAP markers, inflammatory cell markers, and other markers: Cx43, OXR, EP1, EP3, FP, PAR-1, C5a receptor, tryptase, neutrophil elastase, CD68, β-actin, and Na+/K+-ATPase. The immunostaining-positive areas of Cx43, OXR, EP1, EP3, and FP standardized by β-actin in the PAM tissue were significantly smaller than in the control group, whereas those of PAR-1 and Na+/K+-ATPase increased significantly in the PAM group. The Cx43- and OXR-positive areas correlated negatively with the immunostaining-positive cell numbers of CD68 and tryptase with halo, respectively. PAM may impair individual and synchronized myocyte contraction, leading to uterine atony refractory to uterotonics. Further cell-based studies are needed to elucidate the molecular mechanism by which inflammatory cells suppress CAP expression.