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Updated: May 20, 2026
Isolation and Characterization of Human Umbilical Cord-derived Mesenchymal Stem Cells from Preterm and Term Infants
Published on: January 26, 2019
Autophagy markers in umbilical cord blood-derived PBMCs and their association with preterm morbidities: a prospective
Coşkun Armağan1, Can Akyıldız1, Gizem Bakır2
1Faculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.
Insights
Autophagy markers Beclin-1 and LC3B ratio in umbilical cord blood may indicate preterm infant vulnerability. Lower levels are linked to mortality and intraventricular hemorrhage, suggesting impaired autophagy in immature infants.
Area of Science:
- Cellular Biology
- Neonatal Medicine
- Autophagy Research
Background:
- Autophagy is a vital cellular process for maintaining homeostasis under stress.
- Preterm infants face significant oxidative and metabolic stress during the perinatal period.
- Evaluating autophagy markers in preterm infants can reveal insights into neonatal health.
Purpose of the Study:
- To assess levels of autophagy markers (Beclin-1, LC3B-I, LC3B-II) in preterm infants' umbilical cord blood.
- To explore associations between these autophagy markers and major neonatal morbidities and mortality.
Main Methods:
- Prospective multicentre cohort study of 60 preterm infants.
- Western blot analysis of umbilical cord blood for Beclin-1, LC3B-I, and LC3B-II.
- Calculation of LC3B-I/LC3B-II ratio as an indicator of autophagic flux.
- Statistical analysis including Mann-Whitney U tests and multivariable logistic regression adjusted for gestational age.
Main Results:
- Positive correlation between gestational age and Beclin-1 levels.
- Non-survivors showed significantly lower Beclin-1 levels and a depressed LC3B-I/LC3B-II ratio compared to survivors.
- Infants with intraventricular hemorrhage (IVH) had significantly lower LC3B-I levels.
- Adjusted analyses indicated that observed autophagic impairment is linked to gestational immaturity.
Conclusions:
- Lower cord blood Beclin-1 and altered LC3B ratio may serve as markers for preterm infant vulnerability, especially for mortality and IVH.
- Autophagic capacity at birth appears developmentally regulated, with immature infants exhibiting compromised autophagy initiation.
- Findings highlight the role of autophagy in neonatal outcomes and the impact of prematurity.
Introduction:
Autophagy is a crucial cellular degradation pathway that maintains homeostasis during stress. Preterm infants are exposed to significant oxidative and metabolic stress during the perinatal transition. This study aimed to evaluate the levels of autophagy markers (Beclin-1, LC3B-I and LC3B-II) in the umbilical cord blood of preterm infants and investigate their association with neonatal morbidities and mortality.
Material And Methods:
This prospective multicentre cohort study included 60 preterm infants. Umbilical cord blood samples were analysed for Beclin-1, LC3B-I and LC3B-II levels using Western blot. The LC3B-I/LC3B-II ratio was calculated as an indicator of autophagic flux. The relationship between these markers and major neonatal outcomes (respiratory distress syndrome (RDS), intraventricular haemorrhage (IVH), haemodynamically significant patent ductus arteriosus (hsPDA), early neonatal sepsis (ENS) and mortality) was evaluated using Mann-Whitney U tests and multivariable logistic regression adjusted for gestational age.
Results:
A significant positive correlation was observed between gestational age and Beclin-1 levels (r=0.406, p=0.005). In subgroup analyses, non-survivors exhibited significantly lower median Beclin-1 levels (0.45 vs 0.92, p=0.047) and a depressed LC3B-I/LC3B-II ratio (0.48 vs 1.90, p=0.018) compared with survivors. Similarly, infants with IVH had significantly lower LC3B-I levels (0.07 vs 0.65, p=0.011). However, in multivariable logistic regression analyses adjusted for gestational age, the independent statistical significance of these markers was attenuated, suggesting that the observed autophagic impairment is closely linked to gestational immaturity. No significant associations were found for RDS, hsPDA or ENS.
Discussion:
This study identifies lower cord blood Beclin-1 levels and an altered LC3B ratio as potential markers of vulnerability in preterm infants, particularly for mortality and IVH. The findings suggest that autophagic capacity at birth is developmentally regulated, with more immature infants displaying compromised autophagy initiation.
