AI Article Synopsis
- Senescent cells in the placenta release HMGB1, which could influence labor through inflammation, prompting this study to explore the roles of telomere shortening and oxidative damage markers in preterm versus term births.
- A study of 67 placentas showed no significant differences in telomere ratios, HMGB1, or 8-OHdG levels between preterm and term births, although HMGB1 showed a moderate correlation with 8-OHdG levels.
- The findings suggest that, despite the differences in gestational age, preterm placentas may reach a critical telomere length earlier than term placentas, requiring more research to fully understand the relationship between telomere shortening and HMGB1 release in the context of labor
Article Abstract
Introduction: Senescent cells have been demonstrated to release High Mobility Group Box 1 (HMGB1) which induces labor through an inflammatory pathway. This research is aimed at demonstrating whether telomere shortening, proinflammatory HMGB1, and oxidative damage marker 8-OHdG play a role in the placenta of preterm birth in comparison to term birth.
Method: A cross-sectional study on 67 full thickness of the placenta obtained from mothers with term and preterm birth. Mothers with clinical signs of infection (fever > 38°C, leukocytosis > 18000/L, or abnormal vaginal discharge) and other pregnancy complications were excluded. Real-time polymerase chain reaction was performed to measure T/S ratio and ELISA quantification to measure the amount of HMGB1 and 8-OHdG.
Result: A total of 34 placentas from preterm and 33 placentas from term birth were examined. Maternal characteristics were comparable between the two groups. There were no statistical difference of T/S ratio ( = 0.181), HMGB1 ( = 0.119), and 8-OHdG ( = 0.144) between the preterm and term groups. HMGB1 was moderately correlated with 8-OHdG ( = 0.314). Telomere T/S ratio of the placenta did not differ between preterm and term labor despite difference in gestational age, suggesting earlier shortening in the preterm group. It is possible that critical telomere length has been achieved in both term and preterm placenta that warrants labor through senescence process. The result of our study also showed that HMGB1 was not correlated to telomere length, due to the fact that HMGB1 is not upregulated until the critical length of telomere for senescence is exhibited.
Conclusion: Similar telomere length might be exhibited due to early telomere shortening in preterm birth that mimics the term placenta. The relationship between placental telomere shortening and HMGB1 release remains to be uncovered. Further research is needed to discover the factors leading to early telomere shortening in the placenta of preterm birth.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8249137 | PMC |
| http://dx.doi.org/10.1155/2021/9923761 | DOI Listing |
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