open access

Vol 88, No 7 (2017)
Research paper
Published online: 2017-07-31
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The MMP-9/TIMP-1 imbalance and the reduced level of TGF-β in the cervical area of amniotic membrane is a possible risk factor of PROM and premature labor — proof-of-concept study

Małgorzata Litwiniuk1, Małgorzata Radowicka2, Alicja Krejner1, Mirosław Wielgoś2, Tomasz Grzela1
·
Pubmed: 28819943
·
Ginekol Pol 2017;88(7):379-384.
Affiliations
  1. Department of Histology and Embryology, Center for Biostructure Research, Medical University of Warsaw, Warsaw, Poland
  2. 1st Department of Obstetrics and Gynecology, Medical University of Warsaw, Poland

open access

Vol 88, No 7 (2017)
ORIGINAL PAPERS Obstetrics
Published online: 2017-07-31

Abstract

Objectives: To assess the level MMP-9, TIMP-1 and TGF-β in placental and cervical region of amniotic membranes derived from at-term, pre-term and PROM deliveries.

Material and methods: 14 amniotic membranes have been assessed; the quantitative analysis of MMP-9, TGF-β and TIMP-1 was assayed using respective Quantikine Immunoassay Kit.

Results: The MMP-9 level in PROM samples was similar to the level of MMP-9 in at-term membranes and comparable between the cervical and placental region of these membranes. The concentration of TGF-β and TIMP-1 was decreased in the cervical area of AM derived from deliveries complicated with PROM.

Conclusion: The MMP9/TIMP-1 imbalance, as well as the reduced level of TGF-β may be possible risk factors of pre-term labor and PROM.

Abstract

Objectives: To assess the level MMP-9, TIMP-1 and TGF-β in placental and cervical region of amniotic membranes derived from at-term, pre-term and PROM deliveries.

Material and methods: 14 amniotic membranes have been assessed; the quantitative analysis of MMP-9, TGF-β and TIMP-1 was assayed using respective Quantikine Immunoassay Kit.

Results: The MMP-9 level in PROM samples was similar to the level of MMP-9 in at-term membranes and comparable between the cervical and placental region of these membranes. The concentration of TGF-β and TIMP-1 was decreased in the cervical area of AM derived from deliveries complicated with PROM.

Conclusion: The MMP9/TIMP-1 imbalance, as well as the reduced level of TGF-β may be possible risk factors of pre-term labor and PROM.

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Keywords

amniotic membrane, PROM, pre-mature labor, TGF-β

About this article
Title

The MMP-9/TIMP-1 imbalance and the reduced level of TGF-β in the cervical area of amniotic membrane is a possible risk factor of PROM and premature labor — proof-of-concept study

Journal

Ginekologia Polska

Issue

Vol 88, No 7 (2017)

Article type

Research paper

Pages

379-384

Published online

2017-07-31

Page views

1654

Article views/downloads

1279

DOI

10.5603/GP.a2017.0071

Pubmed

28819943

Bibliographic record

Ginekol Pol 2017;88(7):379-384.

Keywords

amniotic membrane
PROM
pre-mature labor
TGF-β

Authors

Małgorzata Litwiniuk
Małgorzata Radowicka
Alicja Krejner
Mirosław Wielgoś
Tomasz Grzela

References (21)
  1. McLaren J, Malak TM, Bell SC. Structural characteristics of term human fetal membranes prior to labour: identification of an area of altered morphology overlying the cervix. Hum Reprod. 1999; 14(1): 237–241.
  2. Malak TM, Bell SC. Structural characteristics of term human fetal membranes: a novel zone of extreme morphological alteration within the rupture site. Br J Obstet Gynaecol. 1994; 101(5): 375–386.
  3. McParland PC, Taylor DJ, Bell SC. Mapping of zones of altered morphology and chorionic connective tissue cellular phenotype in human fetal membranes (amniochorion and decidua) overlying the lower uterine pole and cervix before labor at term. Am J Obstet Gynecol. 2003; 189(5): 1481–1488.
  4. El Khwad M, Stetzer B, Moore RM, et al. Term human fetal membranes have a weak zone overlying the lower uterine pole and cervix before onset of labor. Biol Reprod. 2005; 72(3): 720–726.
  5. El Khwad M, Pandey V, Stetzer B, et al. Fetal membranes from term vaginal deliveries have a zone of weakness exhibiting characteristics of apoptosis and remodeling. J Soc Gynecol Investig. 2006; 13(3): 191–195.
  6. Lei H, Furth EE, Kalluri R, et al. A program of cell death and extracellular matrix degradation is activated in the amnion before the onset of labor. J Clin Invest. 1996; 98(9): 1971–1978.
  7. Manabe Y, Himeno N, Fukumoto M. Tensile strength and collagen content of amniotic membrane do not change after the second trimester or during delivery. Obstet Gynecol. 1991; 78(1): 24–27.
  8. Skinner SJ, Campos GA, Liggins GC. Collagen content of human amniotic membranes: effect of gestation length and premature rupture. Obstet Gynecol. 1981; 57(4): 487–489.
  9. Grzela T, Bikowska B, Litwiniuk M. Matrix metalloproteinases in aortic aneurysm – executors or executioners? In: Grundmann R. ed. Etiology, Pathogenesis and Pathophysiology of Aortic Aneurysms and Aneurysm Rupture. Intech Publ 2011: 25–54.
  10. Fortunato SJ, Menon R, Lombardi SJ. Collagenolytic enzymes (gelatinases) and their inhibitors in human amniochorionic membrane. Am J Obstet Gynecol. 1997; 177(4): 731–741.
  11. Moore RM, Mansour JM, Redline RW, et al. The physiology of fetal membrane rupture: insight gained from the determination of physical properties. Placenta. 2006; 27(11-12): 1037–1051.
  12. Fu X, Parks WC, Heinecke JW. Activation and silencing of matrix metalloproteinases. Semin Cell Dev Biol. 2008; 19(1): 2–13.
  13. Hopkinson A, McIntosh RS, Tighe PJ, et al. Amniotic membrane for ocular surface reconstruction: donor variations and the effect of handling on TGF-beta content. Invest Ophthalmol Vis Sci. 2006; 47(10): 4316–4322.
  14. Litwiniuk M, Radowicka M, Śladowska A. Amount and distribution of selected biologically active factors in amniotic membrane depends on the part of amnion and mode of childbirth. Can we predict properties of amnion dressing? A proof-of-concept study. Centr Eur J Immunol. 2017, accepted for publication.
  15. Faupel-Badger JM, Fichorova RN, Allred EN, et al. Cluster analysis of placental inflammatory proteins can distinguish preeclampsia from preterm labor and premature membrane rupture in singleton deliveries less than 28 weeks of gestation. Am J Reprod Immunol. 2011; 66(6): 488–494.
  16. Xu P, Alfaidy N, Challis JRG. Expression of matrix metalloproteinase (MMP)-2 and MMP-9 in human placenta and fetal membranes in relation to preterm and term labor. J Clin Endocrinol Metab. 2002; 87(3): 1353–1361.
  17. Athayde N, Edwin SS, Romero R, et al. A role for matrix metalloproteinase-9 in spontaneous rupture of the fetal membranes. Am J Obstet Gynecol. 1998; 179(5): 1248–1253.
  18. Locksmith GJ, Clark P, Duff P, et al. Amniotic fluid concentrations of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 during pregnancy and labor. Am J Obstet Gynecol. 2001; 184(2): 159–164.
  19. Vadillo-Ortega F, Hernandez A, Gonzalez-Avila G, et al. Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes. Am J Obstet Gynecol. 1996; 174(4): 1371–1376.
  20. Fortunato SJ, Menon R, Lombardi SJ. MMP/TIMP imbalance in amniotic fluid during PROM: an indirect support for endogenous pathway to membrane rupture. J Perinat Med. 1999; 27(5): 362–368.
  21. Kim GiJ, Romero R, Kuivaniemi H, et al. Expression of bone morphogenetic protein 2 in normal spontaneous labor at term, preterm labor, and preterm premature rupture of membranes. Am J Obstet Gynecol. 2005; 193(3 Pt 2): 1137–1143.

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