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Updated: Nov 2, 2025
Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
Published on: April 30, 2018
Prolactin Protects the Structural Integrity of Human Fetal Membranes by Downregulating Inflammation-induced Secretion
Pilar Flores-Espinosa1, Andrea Olmos-Ortíz1, Martha Granados-Cepeda2
1Immunobiochemistry Branch, INPer IER, Mexico City, Mexico.
Abstract:
Prolactin (PRL) is a pleiotropic hormone with a key role in pregnancy. In fetal membranes, PRL can regulate the secretion of pro-inflammatory factors, which induces the activation of matrix metalloproteinases (MMPs). The increase and activation of MMPs deregulate the turnover of the extracellular matrix in the fetal membranes, altering its structure and function, causing premature rupture of the membranes and preterm labor. In this work, we evaluate the effect of PRL upon the secretion of MMP-1, MMP-2, MMP-9, MMP-13, and the tissue inhibitors of metalloproteinases (TIMPs) in human fetal membranes after lipopolysaccharide (LPS) challenge. Nine fetal membranes from healthy non-laboring cesarean deliveries at term were cultured in a 2-independent chamber system and pre-treated with 250, 500, 1000 or 4000 ng/ml of PRL for 24 h, then choriodecidual region was stimulated with 500 ng/ml of LPS plus fresh PRL for 24 h. The MMPs and TIMPs secretion were quantified by ELISA, additionally MMP-2 and MMP-9 gelatinolytic activity was measured by zymography. LPS induced the MMP-9 and MMP-1 secretion, but no MMP-2 or MMP-13 in comparison with basal levels. PRL co-treatment decreased the MMP-2, MMP-9 and MMP-1 secretion induced by LPS. The active forms were present in the tissue extract, showing a response consistent with the secretion profile. TIMP-1 and TIMP-2 secretion was decreased after LPS treatment and the PRL co-treatment reverts this effect. The present results support that PRL may favor the balance between these factors involved in the structural maintenance of fetal membranes in an inflammatory event.
Insights
Prolactin (PRL) helps maintain fetal membrane integrity during inflammation. This study shows PRL reduces inflammatory matrix metalloproteinases (MMPs) and restores tissue inhibitors of metalloproteinases (TIMPs), preventing preterm labor.
Area of Science:
- Reproductive biology
- Biochemistry
- Cell biology
Background:
- Prolactin (PRL) is crucial in pregnancy and influences fetal membranes.
- Inflammation in fetal membranes can lead to matrix metalloproteinase (MMP) activation, compromising membrane integrity and causing preterm labor.
Purpose of the Study:
- To investigate the effect of prolactin (PRL) on matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in human fetal membranes following lipopolysaccharide (LPS) challenge.
- To determine if PRL can modulate the inflammatory response in fetal membranes.
Main Methods:
- Human fetal membranes were cultured and treated with varying concentrations of PRL.
- Subsequent stimulation with lipopolysaccharide (LPS) was performed.
- Secretion of MMPs and TIMPs was quantified using ELISA, and MMP activity was assessed via zymography.
Main Results:
- LPS induced secretion of MMP-9 and MMP-1, but not MMP-2 or MMP-13.
- PRL co-treatment significantly decreased LPS-induced MMP-2, MMP-9, and MMP-1 secretion.
- LPS reduced TIMP-1 and TIMP-2 secretion, an effect reversed by PRL co-treatment.
Conclusions:
- Prolactin (PRL) plays a protective role in fetal membranes during inflammatory events.
- PRL may help maintain fetal membrane structural integrity by balancing MMPs and TIMPs, potentially preventing preterm labor.
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