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Myofibroblasts accumulate at the rupture site in preterm amniotic membrane after spontaneous PPROM

Eleni Costa, Chris Thrasivoulou, David Laurence Becker

    Fetal Diagnosis and Therapy
    |July 29, 2026
    PubMed
    Abstract

    Insights

    Fetal membranes do not heal after injury, leading to preterm premature rupture of the membranes (PPROM). Myofibroblasts at rupture sites show altered morphology and collagen organization, indicating attempted healing.

    Area of Science:

    • Obstetrics and Gynecology
    • Fetal Medicine
    • Cell Biology

    Background:

    • Fetal membranes lack spontaneous healing capacity after injury, increasing risks of preterm premature rupture of the membranes (PPROM).
    • Understanding the cellular and structural changes at rupture sites is crucial for addressing PPROM.

    Purpose of the Study:

    • To investigate the morphological characteristics of myofibroblasts and collagen organization at the amniotic membrane (AM) rupture site following spontaneous PPROM.
    • To determine if myofibroblasts influence connexin 43 (Cx43) expression at the rupture site.

    Main Methods:

    • Confocal microscopy and second harmonic generation (SHG) imaging were used to analyze AM specimens from women with PPROM.
    • Immunostaining detected alpha-smooth muscle actin (αSMA) and Cx43 in myofibroblasts, with DAPI counterstaining for nuclei.
    • SHG imaging assessed collagen fibril orientation in the fibroblast layer near the rupture.

    Main Results:

    • Rupture sites measured 1.5–4.0 cm in diameter.
    • At rupture edges, αSMA-positive myofibroblasts exhibited deformed nuclei and abundant Cx43 in the cytoplasm or cell-to-cell plaques.
    • Collagen in the fibroblast layer showed degeneration in some areas and polarity near the rupture edge.

    Conclusions:

    • Deformed contractile myofibroblasts and polarized collagen fibrils are present at ruptured membrane sites.
    • Intracellular Cx43 expression and bulbous regions near the epithelial edge suggest attempted re-epithelialization and healing.
    • The precise mechanisms by which myofibroblasts facilitate healing, cell migration, and repair at rupture sites remain to be elucidated.

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