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Heat shock protein 70 expression in neonatal rats after hypoxic stress
E A Ozer1, O Yilmaz, M Akhisaroglu
1Clinics of Pediatrics, SSK Tepecik Teaching Hospital, Izmir, Turkey.
Insights
Premature newborns show diminished heat shock protein 70 (HSP70) expression in the hippocampus following hypoxic stress, suggesting a role in their vulnerability. This age-dependent response was not observed in the heart or kidneys.
Area of Science:
- Neuroscience
- Developmental Biology
- Physiology
Background:
- Hypoxia-induced tissue damage in newborns is age-dependent, with premature infants being more susceptible.
- Heat shock protein 70 (HSP70) is a stress-inducible protein with a known role in cellular protection.
Purpose of the Study:
- To investigate the role of HSP70 in the response to hypoxia in premature versus full-term newborn models.
- To determine if HSP70 expression levels correlate with age-dependent vulnerability to hypoxic insult.
Main Methods:
- Immunohistochemical analysis of HSP70 expression in brain, heart, and kidney tissues.
- Comparison of HSP70 induction in 7-day-old (premature model) and 12-day-old (full-term model) rats subjected to mild hypoxia.
- Control groups exposed to room air for 4 hours.
Main Results:
- HSP70 expression was induced in the hippocampus and myocardium following hypoxia.
- Significantly higher HSP70 levels were observed in the hippocampus of 12-day-old rats compared to 7-day-old rats (p=0.03).
- No significant differences in myocardial HSP70 expression or any significant induction in the kidney were found between age groups or compared to controls.
Conclusions:
- Diminished hippocampal HSP70 expression in premature newborns may contribute to their heightened vulnerability to hypoxic stress.
- HSP70 expression in the heart and kidney following hypoxia does not appear to be directly related to fetal maturity in this model.
Objectives:
The tissue damage due to hypoxia in newborns is to some extent age-dependent; organs of premature babies are more vulnerable to hypoxic insult than full-term neonates. The aim of this immunohistochemical study was to investigate the role of heat shock protein 70 (HSP70), a stress-inducible protein, in developing the response to hypoxia in premature newborns.
Methods:
Postnatal day-7 rats (corresponding to a human fetus of 32-34 weeks' gestation) and day-12 rats (corresponding to a full-term newborn infant) (n = 7) were subjected to mild hypoxia at 33 degrees C. Control rats (n = 7) for each group breathed room air for 4 h. After 4 h of recovery, the animals were killed, and brains, hearts and kidneys were removed for immunohistochemical staining.
Results:
Immunohistochemically, HSP70 expression was found to be induced in the hippocampus and myocardium after exposure to hypoxia. The level of HSP70 expression in the hippocampus after hypoxic stress was significantly higher in the 12-day rats than in the 7-day rats (p = 0.03). However, HSP70 expression in the myocardium did not show any significant difference between the two groups. In addition, no significant induction of HSP70 expression was apparent in the kidney of rats exposed to hypoxia or in any organ of the control animals.
Conclusions:
We conclude that diminished HSP70 expression in the hippocampus of premature newborns may play a critical role in developing the response to hypoxic stress. However, HSP70 expression in the heart and the kidney after exposure to hypoxia did not appear to be related to fetal maturity.