Abstract
Air pollution is one of the largest global environmental health hazards that threaten premature mortality or morbidity. Particulate matter 10 (PM10) has been demonstrated to contribute to several human diseases via dysregulated miRNA expression. Trophoblast cells play a key role in implantation and placentation for a successful pregnancy. Nonetheless, the PM10 associated trophoblast cell functions during pregnancy and miRNA expression are still unknown. Our study showed that PM10 affected HTR-8/SVneo cell viability and also decreased cell proliferation, migration, and invasion. A high concentration of PM10 caused an increase in HTR-8/SVneo cell apoptosis. Treatment with PM10 induced inflammation through the upregulated IL-1β, IL-6, and TNF-α expression in trophoblast cells. In PM10-treated HTR-8/SVneo cells, miR-125b-5p expression was considerably increased and TXNRD1 was found to be negatively related to miR-125b-5p. Collectively, our findings revealed that PM10 could alter miR-125b-5p expression by targeting TXNRD1 and suppressing trophoblast cell functions. Additional investigations relating to the function of miR-125b-5p and its target on particulate pollution exposure in trophoblast are warranted for future biomarker or effective therapeutic approaches.
Highlights
The top five health risks include air pollution with an elevated level of particulate matter (PM), which leads to premature death throughout the globe [1, 2]
To analyze the size and element composition of PM10, samples of PM10 were cut into tiny pieces and identified using scanning electron microscopy (SEM)-energydispersive X-ray system (EDX)
We found that the size distribution of PM10 ranged between 5.2 and 7.0 μm and presented a near-spherical shape (Figure 1)
Summary
The top five health risks include air pollution with an elevated level of particulate matter (PM), which leads to premature death throughout the globe [1, 2]. MiRNAs have been shown to be crucial for cellular functions and human development, including cell proliferation, migration, invasion, differentiation, angiogenesis, and apoptosis [23,24,25]. PM2.5 and PM10 showed a reduction in β-HCG secretion and cell growth, whereas they induced inflammation, endoplasmic reticulum stress, and oxidative stress in the trophoblast cell line [37]. Several investigations have demonstrated that PM2.5 and PM10 alter miRNA expression profiling and are involved in human pathology, including cardiovascular diseases, cancer, neurodegenerative diseases, and pulmonary diseases [40]. We hypothesized that PM10 exposure may modulate trophoblast cell functions through altering trophoblast miRNA expression during an inflammatory response
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