Related Experiment Video
Updated: Feb 2, 2026
Platelet-based Detection of Nitric Oxide in Blood by Measuring VASP Phosphorylation
Published on: January 7, 2019
Alterations in VASP phosphorylation and profilin1 and cofilin1 expression in hyperoxic lung injury and BPD
Mehboob Ali1, Kathryn Heyob2, Trent E Tipple3
1Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, 575 Children's Cross Road, Columbus, OH, USA. mehboob.ali@nationwidechildrens.org.
Insights
Bronchopulmonary dysplasia (BPD) involves altered actin binding proteins in human infants, but not solely due to hyperoxia. This suggests other factors contribute to lung injury repair failure in premature infants.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Neonatology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants, often exacerbated by hyperoxia therapy.
- BPD is characterized by impaired lung repair, reduced cell proliferation, and migration.
- Actin binding proteins (ABPs) regulate essential cellular processes like proliferation and migration.
Purpose of the Study:
- To investigate the role of ABPs and lung mesenchymal stem cells (L-MSCs) in hyperoxia-induced lung injury and repair in BPD.
- To explore the expression and function of VASP, cofilin1, and profilin1 in the context of BPD pathophysiology.
- To compare findings in human BPD tissues with a murine model of neonatal hyperoxia.
Main Methods:
- Immunofluorescence and western blot analyses were used to assess ABP and CD146+ L-MSC expression.
- Human lung autopsy tissues from infants with and without BPD were examined.
- A murine model of neonatal hyperoxia-induced lung injury was employed for comparative analysis.
Main Results:
- Human BPD lung tissues showed decreased F-actin, altered VASP phosphorylation, and reduced profilin 1 expression.
- Increased cofilin 1 expression was observed in both human and mouse lung tissues at 7 days post-exposure.
- Elevated CD146 levels were noted in both human and mouse tissues.
Conclusions:
- Dysregulation of VASP, profilin 1, and cofilin 1 in human tissues suggests their involvement in BPD pathophysiology.
- The absence of similar changes in the mouse model indicates that factors beyond hyperoxia alone may disrupt ABP expression in BPD.
- Further research is needed to elucidate the precise mechanisms and contributing factors in BPD-related lung injury and repair.
Background:
Hyperoxia is a frequently employed therapy for prematurely born infants, induces lung injury and contributes to development of bronchopulmonary dysplasia (BPD). BPD is characterized by decreased cellular proliferation, cellular migration, and failure of injury repair systems. Actin binding proteins (ABPs) such as VASP, cofilin1, and profilin1 regulate cell proliferation and migration via modulation of actin dynamics. Lung mesenchymal stem cells (L-MSCs) initiate repair processes by proliferating, migrating, and localizing to sites of injury. These processes have not been extensively explored in hyperoxia induced lung injury and repair.
Methods:
ABPs and CD146+ L-MSCs were analyzed by immunofluorescence in human lung autopsy tissues from infants with and without BPD and by western blot in lung tissue homogenates obtained from our murine model of newborn hyperoxic lung injury.
Results:
Decreased F-actin content, ratio of VASPpS157/VASPpS239, and profilin 1 expression were observed in human lung tissues but this same pattern was not observed in lungs from hyperoxia-exposed newborn mice. Increases in cofilin1 expression were observed in both human and mouse tissues at 7d indicating a dysregulation in actin dynamics which may be related to altered growth. CD146 levels were elevated in human and newborn mice tissues (7d).
Conclusion:
Altered phosphorylation of VASP and expression of profilin 1 and cofilin 1 in human tissues indicate that the pathophysiology of BPD involves dysregulation of actin binding proteins. Lack of similar changes in a mouse model of hyperoxia exposure imply that disruption in actin binding protein expression may be linked to interventions or morbidities other than hyperoxia alone.
More Related Videos
08:58Development of a Neonatal Piglet Acute Lung Injury Model Recreating the Early Environment of Preterm Infant Lungs
Published on: October 31, 2025
09:16Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury
Published on: February 26, 2017
Related Concept Videos
01:02Phosphorylation
During phosphorylation, protein kinases transfer the terminal phosphate group of ATP to specific amino acid side chains of substrate proteins. Serine, threonine, and tyrosine are the most commonly...
01:30Alterations in Respiration II
In Biot's breathing, the respiratory rate and depth are irregular, alternating between periods of deep gasping and apnea. Common causes...
01:06Altered States of Awareness
The ingestion of substances like stimulants or hallucinogens leads to chemical alterations in the brain...
01:47Lung Capacity
01:42What is Gene Expression?
Gene expression is the process in which DNA directs the synthesis of functional products, that is, proteins. Cells can regulate gene expression at various stages. It allows organisms to generate different cell types and enables cells to adapt to internal and external factors.
Genetic Information Flows from DNA to RNA to Protein
A gene is a stretch of DNA that serves as the blueprint for functional RNAs and proteins. Since DNA is made up of nucleotides and proteins consist of amino...
01:30Alterations in Blood Pressure
Hypertension (High blood pressure)
Hypertension occurs when blood pressure readings consistently exceed the normal range. It is diagnosed when systolic blood pressure (the top number, indicating pressure while the heart...