Role of tumor necrosis factor-α in the premature rupture of membranes and preterm labor pathways

Role of tumor necrosis factor-α in the premature rupture of membranes and preterm labor pathways
复制标题

DOI:
10.1067/mob.2002.127457
复制
发表时间:
2002-11-01
影响因子:
9.8
通讯作者:
Lombardi, SJ
Lombardi, SJ
中科院分区:
医学1区
文献类型:
--
作者:
Fortunato, SJ;Menon, R;Lombardi, SJ

文献摘要

被引文献

相似文献

目的:为了进一步描绘早产和膜途径的过早破裂之间的差异,我们研究了炎症细胞因子作为基质金属蛋白酶2和9的激活剂在人类fetal membranes.Study Design:正常的绒毛膜是保持在器官外植体系统的作用,刺激白细胞介素-1 β,肿瘤坏死因子-α,或白细胞介素-6。用逆转录-聚合酶链反应和特异性底物活性测定法检测基质金属蛋白酶2和9在绒毛膜中的表达和活性。基质金属蛋白酶抑制剂,金属蛋白酶的组织抑制剂-1,浓度测定通过酶联免疫吸附试验。结果:白细胞介素-1 β,肿瘤坏死因子-α,白细胞介素-6诱导的表达基质金属蛋白酶-9信使RNA,而基质金属蛋白酶-2的表达是组成性的控制和姜黄素刺激的组织。基质金属蛋白酶-2活性在细胞因子刺激后没有变化。活性基质金属蛋白酶-9在肿瘤坏死因子刺激的组织中显着升高,而在白细胞介素-1或白细胞介素-6刺激后则没有变化。基质金属蛋白酶组织抑制因子-1水平下降后,白细胞介素-1和肿瘤坏死因子刺激,但改变后,白细胞介素-6 stimulation.CONCLUSION:只有肿瘤坏死因子-α增加基质金属蛋白酶-9活性在绒毛膜。
OBJECTIVE: To further delineate the differences between the preterm labor and premature rupture of the membrane pathways, we investigated the role of the inflammatory cytokines as activators of matrix metalloproteinases 2 and 9 in human fetal membranes.STUDY DESIGN: Normal amniochorionic membrane that is maintained in an organ explant system was stimulated with interleukin-1beta, tumor necrosis factor-alpha, or interleukin-6. The expression and activity of matrix metalloproteinases 2 and 9 in amniochorion was documented with reverse transcriptase-polymerase chain reaction and specific substrate activity assays. The matrix metalloproteinase inhibitor, tissue inhibitor of metalloproteinase-1, concentration was measured by enzyme-linked immunosorbent assay.RESULTS: Interleukin-1beta, tumor necrosis factor-alpha, and interleukin-6 induced the expression of matrix metalloproteinase-9 messenger RNA, whereas matrix metalloproteinase-2 expression was constitutive in control and cytokine-stimulated tissues. Matrix metalloproteinase-2 activity did not change after cytokine stimulation. Active matrix metalloproteinase-9 was significantly higher in tumor necrosis factor-stimulated tissues, which conversely were not changed after interleukin-1 or interleukin-6 stimulation. Tissue inhibitor of metalloproteinase-1 levels were decreased after interleukin-1 and tumor necrosis factor stimulation but changed-after interleukin-6 stimulation.CONCLUSION: Only tumor necrosis factor-alpha increases matrix metalloproteinase-9 activity in amniochorion.