title: [Role of matrix metalloproteinase-2,9 and their inhibitors in premature rupture of membranes].
abstract: OBJECTIVE
  To investigate the role of matrix metalloproteinase-2,9 (MMP-2, MMP-9) and tissue inhibitor of matrix metalloproteinases-2,1 (TIMP-2, TIMP-1) in human amniochorionic membrane.
  
  
  METHODS
  Amniochorionic membranes were collected from the following groups of women: (1) women with spontaneous premature rupture of membrane (PROM) before onset of labor (PROM group, n = 8), (2) Women with term labor after vaginal delivery (vaginal delivery group, n = 8), (3) Women undergoing elective cesarean section (C-section group, n = 8). Messenger ribonucleic acid expression for MMP-2, MMP-9, and their specific inhibitors TIMP-2 and TIMP-1 were studied with reverse transcriptase polymerase chain reaction.
  
  
  RESULTS
  (1) MMP-2 level in PROM group was 0.849 +/- 0.037; in vaginal delivery group 0.327 +/- 0.023; in C-section group 0.307 +/- 0.028. Expression in PROM group was highest, with significant difference compared with the other groups (P < 0.05). Its expression in vaginal delivery group and C-section group had no significant difference (P > 0.05). (2) MMP-9 level in PROM group was 0.026 +/- 0.004; in vaginal delivery group 0.008 +/- 0.001, with significant difference between the two groups (P < 0.05), while the expression was absent in C-section group. (3) TIMP-2 level in PROM group was 0.420 +/- 0.122; in vaginal delivery group 0.730 +/- 0.148; in C-section group 0.885 +/- 0.065. The expression in PROM group was significantly lower than in vaginal delivery group and C-section group (P < 0.05). And it was significantly lower in vaginal delivery group than in C-section group (P < 0.05). (4)TIMP-1 level in PROM group was 0.442 +/- 0.020; in vaginal delivery group 0.431 +/- 0.016; in C-section group 0.427 +/- 0.011. The expression in three groups had no significant difference (P > 0.05).
  
  
  CONCLUSIONS
  In PROM group, the expression of MMP-2, MMP-9 and their inhibitors TIMP-2, TIMP-1 is imbalanced, leading to increased extracellular matrix degradation, and weakening of the fetal membranes, and eventually premature rupture of the membranes.
authors.affiliation: Department of Obstetrics and Gynecology, Zhongnan Hospital, Wuhan University, Wuhan 430071, China.
authors.forename: Hong-lin
authors.initials: HL
authors.lastname: Wang
authors.forename: Chun
authors.initials: C
authors.lastname: Zhou
authors.forename: Yuan-zhen
authors.initials: YZ
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000653:Amniotic Fluid / Q000201:enzymology / Q000378:metabolism; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000201:enzymology*; D006801:Humans; D007743:Labor, Obstetric; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis / Q000235:genetics; D020782:Matrix Metalloproteinases / Q000096:biosynthesis* / Q000235:genetics; D010920:Placenta / Q000201:enzymology; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000096:biosynthesis / Q000235:genetics; D019714:Tissue Inhibitor of Metalloproteinases / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D012333:RNA, Messenger; D019714:Tissue Inhibitor of Metalloproteinases; D019716:Tissue Inhibitor of Metalloproteinase-2; D020782:Matrix Metalloproteinases; D020780:Matrix Metalloproteinase 9