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The role of matrix degrading enzymes and apoptosis in rupture of membranes.
- Source :
-
Journal of the Society for Gynecologic Investigation [J Soc Gynecol Investig] 2004 Oct; Vol. 11 (7), pp. 427-37. - Publication Year :
- 2004
-
Abstract
- Prematurity is the third leading cause of perinatal death, and preterm premature rupture of the membranes (pPROM) is associated with approximately 20-50% of all preterm births. The etiologic factors described for pPROM and preterm labor (PTL) are the same, although the clinical presentation (pPROM vs PTL) differs among patients. The reason for this disparity is unknown and poses a therapeutic dilemma. Several etiologic factors have been described for PTL and pPROM. PTL and pPROM are associated with overwhelming host inflammatory response. Many of these pro-inflammatory factors (inflammatory cytokine release) are common in both conditions; however, the clinical presentation differs. The objective of this review is to explain the differential expression pattern of matrix metalloproteinases (MMPs) and pro-apoptotic elements in human fetal membranes in pPROM and PTL and how they interact to present different clinical outcomes during pregnancy.
- Subjects :
- Bacteria enzymology
Extraembryonic Membranes pathology
Extraembryonic Membranes physiopathology
Female
Fetal Membranes, Premature Rupture microbiology
Humans
Matrix Metalloproteinase 2 physiology
Matrix Metalloproteinase Inhibitors
Obstetric Labor, Premature enzymology
Obstetric Labor, Premature microbiology
Obstetric Labor, Premature pathology
Peptide Hydrolases physiology
Pregnancy
Apoptosis physiology
Fetal Membranes, Premature Rupture enzymology
Fetal Membranes, Premature Rupture pathology
Matrix Metalloproteinases physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1071-5576
- Volume :
- 11
- Issue :
- 7
- Database :
- MEDLINE
- Journal :
- Journal of the Society for Gynecologic Investigation
- Publication Type :
- Academic Journal
- Accession number :
- 15458739
- Full Text :
- https://doi.org/10.1016/j.jsgi.2004.04.001