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VIP/PACAP signaling as an alternative target during hyperoxic exposure in preterm newborns
1Department of Biology, Faculty of Medicine, University of Prishtina, Prishtina, Kosovo. qendrimthaqi214@hotmail.com, Institute of Biology, Faculty of Natural Science and Mathematics, Ss Cyril and Methodius University, Skopje, North Macedonia. m.mitko@gmail.com.
Insights
High oxygen therapy (hyperoxia) saves premature infants but causes lung disease. This study explores how hyperoxia affects airway smooth muscle relaxation, focusing on vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating peptide (PACAP).
Area of Science:
- Neonatal Physiology
- Respiratory Medicine
- Molecular Biology
Background:
- Hyperoxia (high oxygen) is crucial for premature infant survival but causes bronchopulmonary dysplasia.
- Hyperoxia leads to airway hyper-responsiveness and impaired smooth muscle relaxation, partly due to reduced nitric oxide.
- Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating peptide (PACAP) are critical for regulating airway caliber.
Purpose of the Study:
- To investigate the role of VIP and PACAP in regulating airway and tracheal smooth muscle contractility during hyperoxic exposure in preterm neonates.
- To understand the mechanisms underlying hyperoxia-induced airway hyper-reactivity.
Main Methods:
- In vivo and in vitro studies of airway smooth muscle function.
- Assessment of nitric oxide release.
- Evaluation of VIP and PACAP signaling pathways in hyperoxic conditions.
Main Results:
- Hyperoxia impairs airway smooth muscle relaxation by reducing nitric oxide release.
- The VIP/PACAP pathway's role in hyperoxia-induced airway contractility in preterm neonates is not well understood.
- Further research is needed to elucidate the specific mechanisms.
Conclusions:
- Hyperoxia significantly impacts airway smooth muscle function in premature infants.
- Understanding the VIP/PACAP pathway's involvement is crucial for developing targeted therapies for bronchopulmonary dysplasia.
- This study highlights a potential therapeutic target for mitigating hyperoxia-induced lung injury.
Abstract:
The use of oxygen therapy (high doses of oxygen - hyperoxia) in the treatment of premature infants results in their survival. However, it also results in a high incidence of chronic lung disease known as bronchopulmonary dysplasia, a disease in which airway hyper-responsiveness and pulmonary hypertension are well known as consequences. In our previous studies, we have shown that hyperoxia causes airway hyper-reactivity, characterized by an increased constrictive and impaired airway smooth muscle relaxation due to a reduced release of relaxant molecules such as nitric oxide, measured under in vivo and in vitro conditions (extra- and intrapulmonary) airways. In addition, the relaxation pathway of the vasoactive intestinal peptide (VIP) and/or pituitary adenylate cyclase activating peptide (PACAP) is another part of this system that plays an important role in the airway caliber. Peptide, which activates VIP cyclase and pituitary adenylate cyclase, has prolonged airway smooth muscle activity. It has long been known that VIP inhibits airway smooth muscle cell proliferation in a mouse model of asthma, but there is no data about its role in the regulation of airway and tracheal smooth muscle contractility during hyperoxic exposure of preterm newborns.
