TY - JOUR
T1 - Oxidative Stress Induced Damage and Early Senescence in Preterm Placenta
AU - Saroyo, Yudianto Budi
AU - Wibowo, Noroyono
AU - Irwinda, Rima
AU - Prijanti, Ani Retno
AU - Yunihastuti, Evy
AU - Bardosono, Saptawati
AU - Krisnadi, Sofie Rifayani
AU - Permata, Putri Indah
AU - Wijaya, Stephanie
AU - Santawi, Victor Prana Andika
N1 - Funding Information:
Special thanks are due to the Prodia laboratory team for their transparency and explanation on every step of laboratory work conducted during the study. This study is funded by the Ministry of Research and Technology, Indonesian Government.
Publisher Copyright:
© 2021 Yudianto Budi Saroyo et al.
PY - 2021
Y1 - 2021
N2 - 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/μL, 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 (p=0.181), HMGB1 (p=0.119), and 8-OHdG (p=0.144) between the preterm and term groups. HMGB1 was moderately correlated with 8-OHdG (r=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.
AB - 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/μL, 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 (p=0.181), HMGB1 (p=0.119), and 8-OHdG (p=0.144) between the preterm and term groups. HMGB1 was moderately correlated with 8-OHdG (r=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.
UR - http://www.scopus.com/inward/record.url?scp=85109338598&partnerID=8YFLogxK
U2 - 10.1155/2021/9923761
DO - 10.1155/2021/9923761
M3 - Article
AN - SCOPUS:85109338598
SN - 2090-2727
VL - 2021
JO - Journal of Pregnancy
JF - Journal of Pregnancy
M1 - 9923761
ER -