The Role of Prostaglandins in the Mechanism of Lipopolysaccharide-Induced proMMP9 Secretion from Human Placenta and Fetal Membrane Cells
Bibliographic record
Abstract
The abnormal degradation of the extracellular matrix by matrix metalloproteinases (MMPs) in the fetal membranes has been proposed as a central event in preterm premature rupture of the membranes (pPROM). Prostaglandins (PGs) are thought to increase the risk of preterm premature rupture of the fetal membranes by causing matrix degradation. The aim of this study was to assess the mediating role of PGs on lipopolysaccharide (LPS)-induced MMP9 secretion in vitro. ELISA, zymography, and Western blotting were performed on cells and medium from cultures of purified chorion trophoblasts (CTs) and syncytiotrophoblasts (STs) from the human placenta and fetal membranes treated with LPS, meloxicam, (a selective prostaglandin-endoperoxide synthase 2 [PTGS2, previously known as cyclooxygenase 2] inhibitor), or replacement PGE(2) or PGF(2alpha). LPS significantly (P < 0.01) increased proMMP9 secretion and prostaglandin E(2) (PGE(2)) output by cultured CTs and STs, but there was no effect on tissue inhibitor of matrix metalloproteinase 1 (TIMP1) secretion. In these cells, meloxicam significantly blocked LPS-induced proMMP9 secretion and PGE(2) output (P < 0.01). Exogenous PGE(2) and PGF(2alpha) significantly reversed the reduction in proMMP9 secretion caused by meloxicam in a dose-dependent manner (P < 0.01). The expression of PTGS2 protein in CTs and STs was increased dramatically after LPS treatment, but there was no significant effect on the expression of PTGS1 (previously known as cyclooxygenase 1), membrane-associated prostaglandin E synthases (membrane-associated PTGES, previously known as mPGES) 1 and 2, or cytosolic prostaglandin E synthase (cytosolic PTGES, previously knows as cPGES) proteins. Our results suggest that PGs may mediate the selective increase in MMP9 after exposure of trophoblast cells to LPS. There was no effect of LPS on TIMP1. Understanding this relationship may help in developing strategies for the prevention and management of pPROM and preterm labor.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".