Walsh Scott W, Nugent William H, Solotskaya Anna V, Anderson Charles D, Grider John R, Strauss Jerome F
1 Department of Obstetrics and Gynecology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
2 Department of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Reprod Sci. 2018 Jul;25(7):1058-1066. doi: 10.1177/1933719117732162. Epub 2017 Sep 27.
Matrix metalloproteinase-1 (MMP-1) and neutrophil elastase are proteolytic enzymes involved in tissue remodeling, but a role for them as uterotonic agents has not been considered. However, both these proteases activate protease-activated receptor 1 (PAR-1) that mediates thrombin-induced contractions. Matrix metalloproteinase-1 and elastase are products of neutrophils that infiltrate intrauterine tissues at the time of labor, so we tested the hypothesis that these proteases might be novel uterotonic agents acting via PAR-1. Decidual tissue was collected from fetal membranes of term not-in-labor (TNL), term labor (TL), and preterm labor (PTL) women and analyzed for gene and protein expression of MMP-1 and neutrophil elastase. Contractile effects of MMP-1 and elastase were tested with uterine strips of day 19 and 20 gestation rats. Expression of MMP-1 and neutrophil elastase was increased in TL and PTL as compared to TNL. Expression of both the pro- and active enzymes of MMP-1 increased progressively from TNL to TL to PTL. Tumor necrosis factor-α, a neutrophil product, increased MMP-1 in decidual and myometrial cells. Both MMP-1 and elastase stimulated strong contractions of myometrial strips, which were prevented by inhibition of PAR-1 and inhibition of inositol trisphosphate receptor or calcium channel blockade. Indomethacin did not prevent protease-induced contractions. These data suggest that MMP-1 and neutrophil elastase may be important but heretofore unrecognized players in stimulating uterine contractions at the time of labor, and they may explain why indomethacin delays, but does not prevent, PTL because indomethacin inhibits the prostaglandin component but not the protease component of labor.
基质金属蛋白酶-1(MMP-1)和中性粒细胞弹性蛋白酶是参与组织重塑的蛋白水解酶,但它们作为宫缩剂的作用尚未得到考虑。然而,这两种蛋白酶均可激活介导凝血酶诱导收缩的蛋白酶激活受体1(PAR-1)。MMP-1和弹性蛋白酶是中性粒细胞的产物,在分娩时浸润子宫内组织,因此我们测试了以下假设:这些蛋白酶可能是通过PAR-1起作用的新型宫缩剂。从足月未临产(TNL)、足月临产(TL)和早产(PTL)妇女的胎膜中收集蜕膜组织,并分析MMP-1和中性粒细胞弹性蛋白酶的基因和蛋白表达。用妊娠第19天和20天大鼠的子宫条测试MMP-1和弹性蛋白酶的收缩作用。与TNL相比,TL和PTL中MMP-1和中性粒细胞弹性蛋白酶的表达增加。MMP-1的前体酶和活性酶的表达从TNL到TL再到PTL逐渐增加。中性粒细胞产物肿瘤坏死因子-α增加了蜕膜和子宫肌层细胞中的MMP-1。MMP-1和弹性蛋白酶均刺激子宫肌层条强烈收缩,而PAR-1的抑制、肌醇三磷酸受体的抑制或钙通道阻滞剂可阻止这种收缩。吲哚美辛不能阻止蛋白酶诱导的收缩。这些数据表明,MMP-1和中性粒细胞弹性蛋白酶可能是分娩时刺激子宫收缩的重要但此前未被认识的因素,它们可能解释了为什么吲哚美辛会延迟但不能预防PTL,因为吲哚美辛抑制了分娩的前列腺素成分而非蛋白酶成分。