Frontiers in cell and developmental biology · 2026
Fluid percussion trauma to the placental trophoblast triggers multifaceted injury mechanisms, including mitochondrial stress response, immune dysregulation, cytoskeletal, endothelial, and angiogenic signaling cascades.
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Paidas Michael J, West Emily M, Speciale Anna Rosa, Patel Urja C, Ramamoorthy Rajalakshmi, Kumar Swati, Patrizio Rebecca, Belkin Elise Michelle, Attia Christina, Shaikh Aleezeh, Kandasamy Ganapathi, Ahmad Nayab, Porter Edna, Ahmad Anis, Jayakumar Arumugam R
Аннотация
INTRODUCTION: Trauma is the leading cause of non-obstetrical maternal death and is linked to adverse pregnancy outcomes, including placental abruption, preterm birth, and stillbirth. Although placental injury is a known consequence of maternal trauma, understanding its direct effect on trophoblast function remains limited. This study aims to examine the cellular effects of mechanical trauma on human trophoblasts in vitro.
METHODS: Human trophoblast cells (HTR-8/SVneo) were cultured and exposed to controlled mechanical trauma using a fluid percussion injury (FPI) model, previously validated in traumatic brain injury research. Cell viability was measured 48 h after injury with a fluorometric assay kit. Immunofluorescence and Western blot analyses were carried out to assess the levels of mitochondrial markers (TOM20, COX1, VDAC1) and the antiangiogenic factor sFlt-1.
RESULTS: Trophoblasts subjected to trauma exhibited reduced viability compared with controls. Expression of sFlt-1 and SDHA increased in injured cells, indicating a cellular stress response. Western blot results revealed a twofold decrease in TOM20 levels and a slight reduction in VDAC1 levels, while COX1 levels remained unchanged. Moreover, next-generation sequencing of trophoblasts after trauma showed altered gene expression involving several injury pathways, including mitochondrial stress response, immune dysregulation, cytoskeletal changes, endothelial and angiogenic signaling pathways, calcium signaling, metabolic imbalance, and inflammation. These results suggest that mechanical trauma causes mitochondrial dysfunction and disrupts angiogenic signaling in trophoblasts.
DISCUSSION: Trauma induces significant mitochondrial changes and cellular stress, characterized by reduced viability, decreased TOM20 and VDAC1 levels, and increased sFlt-1 and SDHA levels. These patterns resemble those seen in hypoxia-related placental disorders such as preeclampsia, fetal distress, and placental abruption. Understanding these mechanisms may help clarify how maternal trauma contributes to adverse pregnancy outcomes. Further studies using in vivo models are required to explore the clinical relevance of these findings.
METHODS: Human trophoblast cells (HTR-8/SVneo) were cultured and exposed to controlled mechanical trauma using a fluid percussion injury (FPI) model, previously validated in traumatic brain injury research. Cell viability was measured 48 h after injury with a fluorometric assay kit. Immunofluorescence and Western blot analyses were carried out to assess the levels of mitochondrial markers (TOM20, COX1, VDAC1) and the antiangiogenic factor sFlt-1.
RESULTS: Trophoblasts subjected to trauma exhibited reduced viability compared with controls. Expression of sFlt-1 and SDHA increased in injured cells, indicating a cellular stress response. Western blot results revealed a twofold decrease in TOM20 levels and a slight reduction in VDAC1 levels, while COX1 levels remained unchanged. Moreover, next-generation sequencing of trophoblasts after trauma showed altered gene expression involving several injury pathways, including mitochondrial stress response, immune dysregulation, cytoskeletal changes, endothelial and angiogenic signaling pathways, calcium signaling, metabolic imbalance, and inflammation. These results suggest that mechanical trauma causes mitochondrial dysfunction and disrupts angiogenic signaling in trophoblasts.
DISCUSSION: Trauma induces significant mitochondrial changes and cellular stress, characterized by reduced viability, decreased TOM20 and VDAC1 levels, and increased sFlt-1 and SDHA levels. These patterns resemble those seen in hypoxia-related placental disorders such as preeclampsia, fetal distress, and placental abruption. Understanding these mechanisms may help clarify how maternal trauma contributes to adverse pregnancy outcomes. Further studies using in vivo models are required to explore the clinical relevance of these findings.