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Preterm premature rupture of membranes without labor is not associated with increased levels of matrix metalloproteinase-9 protein.未临产的胎膜早破与基质金属蛋白酶-9蛋白水平升高无关。
Prenat Neonatal Med. 2001 Aug 1;6(4):219-226.
2
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A role for the 72 kDa gelatinase (MMP-2) and its inhibitor (TIMP-2) in human parturition, premature rupture of membranes and intraamniotic infection.72 kDa明胶酶（基质金属蛋白酶-2，MMP-2）及其抑制剂（金属蛋白酶组织抑制因子-2，TIMP-2）在人类分娩、胎膜早破及羊膜腔内感染中的作用。
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Fetal plasma MMP-9 concentrations are elevated in preterm premature rupture of the membranes.胎膜早破早产时胎儿血浆基质金属蛋白酶-9浓度升高。
Am J Obstet Gynecol. 2002 Nov;187(5):1125-30. doi: 10.1067/mob.2002.127312.
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Expression of NOD1 and downstream factors in placenta, fetal membrane and plasma from pregnancies with premature rupture of membranes and their significance.胎膜早破孕妇胎盘、胎膜及血浆中NOD1及其下游因子的表达及其意义
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Evaluation of the expression and enzyme activity of matrix metalloproteinase-7 in fetal membranes during premature rupture of membranes at term in humans.足月胎膜早破时人胎膜中基质金属蛋白酶-7的表达及酶活性评估
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MMP/TIMP imbalance in amniotic fluid during PROM: an indirect support for endogenous pathway to membrane rupture.胎膜早破时羊水内基质金属蛋白酶/金属蛋白酶组织抑制因子失衡：对胎膜破裂内源性途径的间接支持
J Perinat Med. 1999;27(5):362-8. doi: 10.1515/JPM.1999.049.

本文引用的文献

1
Amniotic fluid matrix metalloproteinase-9 levels in women with preterm labor and suspected intra-amniotic infection.
Obstet Gynecol. 1999 Jul;94(1):1-6. doi: 10.1016/s0029-7844(99)00011-3.
2
Premature rupture of the fetal membranes.胎膜早破
N Engl J Med. 1998 Mar 5;338(10):663-70. doi: 10.1056/NEJM199803053381006.
3
Collagenolytic enzymes (gelatinases) and their inhibitors in human amniochorionic membrane.人羊膜绒毛膜中的胶原水解酶（明胶酶）及其抑制剂
Am J Obstet Gynecol. 1997 Oct;177(4):731-41. doi: 10.1016/s0002-9378(97)70260-6.
4
HL-60 leukemia cells produce an autocatalytically truncated form of matrix metalloproteinase-9 with impaired sensitivity to inhibition by tissue inhibitors of metalloproteinases.HL-60白血病细胞产生一种基质金属蛋白酶-9的自催化截短形式，对金属蛋白酶组织抑制剂的抑制敏感性受损。
Leukemia. 1996 Sep;10(9):1520-6.
5
Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes.妊娠合并胎膜早破孕妇羊水的基质金属蛋白酶活性增加及金属蛋白酶组织抑制因子-1水平降低。
Am J Obstet Gynecol. 1996 Apr;174(4):1371-6. doi: 10.1016/s0002-9378(96)70687-7.
6
Confocal immunofluorescence localization of collagen types I, III, IV, V and VI and their ultrastructural organization in term human fetal membranes.足月人胎膜中I、III、IV、V和VI型胶原蛋白的共聚焦免疫荧光定位及其超微结构组织
Placenta. 1993 Jul-Aug;14(4):385-406. doi: 10.1016/s0143-4004(05)80460-6.
7
Structural characteristics of term human fetal membranes: a novel zone of extreme morphological alteration within the rupture site.足月人胎膜的结构特征：破裂部位内一个形态学改变极为显著的新区域。
Br J Obstet Gynaecol. 1994 May;101(5):375-86. doi: 10.1111/j.1471-0528.1994.tb11908.x.
8
92-kd type IV collagenase (matrix metalloproteinase-9) activity in human amniochorion increases with labor.人羊膜绒毛膜中92-kd IV型胶原酶（基质金属蛋白酶-9）的活性随分娩而增加。
Am J Pathol. 1995 Jan;146(1):148-56.
9
Control of peripartal collagenolysis in the human chorion-decidua.人绒毛膜 - 蜕膜中围产期胶原溶解的控制
Am J Obstet Gynecol. 1995 Jan;172(1 Pt 1):63-70. doi: 10.1016/0002-9378(95)90085-3.
10
Leukemic cells (HL-60) produce a novel extracellular matrix-degrading proteinase that is not inhibited by tissue inhibitors of matrix metalloproteinases (TIMPs).白血病细胞（HL-60）产生一种新型的细胞外基质降解蛋白酶，该酶不受基质金属蛋白酶组织抑制剂（TIMPs）的抑制。
Exp Hematol. 1995 Feb;23(2):155-60.

未临产的胎膜早破与基质金属蛋白酶-9蛋白水平升高无关。

Preterm premature rupture of membranes without labor is not associated with increased levels of matrix metalloproteinase-9 protein.

作者信息

Draper D L, Kush M J, Donohoe W, Janosky J, Latimer J J, Heine R P

机构信息

Magee-Women's Research Institute, Department of Obstetrics and Gynecology and Reproductive Sciences, School of Medicine, University of Pittsburgh, Pennsylvania, USA.

Magee-Women's Research Institute, Department of Family Medicine and Clinical Epidemiology, School of Medicine, University of Pittsburgh, Pennsylvania, USA.

出版信息

Prenat Neonatal Med. 2001 Aug 1;6(4):219-226.

PMID:26924938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4769030/
Abstract

OBJECTIVES

Preterm premature rupture of membranes (PROM) accounts for 30-40% of all preterm births. The objectives of this study were to determine whether matrix metalloproteinase-9 (MMP-9) is increased in preterm PROM fetal membranes, whether labor or gestational age affects expression, and whether the increase is localized to the rupture site or is membrane-wide.

METHODS

Fetal membranes were collected from 15 pregnancies complicated by preterm PROM and 26 control cases, which delivered at term or preterm without PROM. The preterm PROM cases represented both patients who labored and those who did not. Membrane samples at the rupture site and a remote site (approximately > 5 cm) were analyzed for MMP-9 protein and enzymatic activity by Western blot and gelatin zymography, respectively.

RESULTS

MMP-9 levels in fetal membranes were similar at both the rupture and the remote sites. The highest levels of total MMP-9 protein were found in preterm PROM patients with labor ( < 0.05) and were increased four-fold over protein levels in non-laboring preterm PROM patients delivered by Cesarean section ( < 0.001). In preterm PROM patients without labor, levels of MMP-9 protein were similar to those of non-laboring patients at term and preterm. Zymography correlated with protein results in all membranes.

CONCLUSIONS

Preterm PROM without labor is not associated with increased membrane levels of MMP-9 protein, suggesting that its local elevation does not play a role in early membrane rupture.

摘要

目的

胎膜早破（PROM）占所有早产的30%-40%。本研究的目的是确定基质金属蛋白酶-9（MMP-9）在早产PROM胎儿胎膜中是否升高，分娩或孕周是否影响其表达，以及这种升高是局限于破裂部位还是全膜范围。

方法

收集15例并发早产PROM的妊娠病例及26例足月或早产未发生PROM的对照病例的胎儿胎膜。早产PROM病例包括已分娩和未分娩的患者。分别通过蛋白质印迹法和明胶酶谱法分析破裂部位和远处部位（约>5 cm）的胎膜样本中的MMP-9蛋白和酶活性。

结果

胎膜中MMP-9水平在破裂部位和远处部位相似。在已分娩的早产PROM患者中发现总MMP-9蛋白水平最高（<0.05），比剖宫产分娩的未分娩早产PROM患者的蛋白水平增加了四倍（<0.001）。在未分娩的早产PROM患者中，MMP-9蛋白水平与足月和早产未分娩患者相似。酶谱分析结果与所有胎膜的蛋白质结果相关。

结论

未分娩的早产PROM与胎膜中MMP-9蛋白水平升高无关，提示其局部升高在胎膜早期破裂中不起作用。