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