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Published on: October 22, 2019
A critical regulatory role for macrophage migration inhibitory factor in hyperoxia-induced injury in the developing
Huanxing Sun1, Rayman Choo-Wing, Angara Sureshbabu
1Department of Pediatrics, Yale University, New Haven, Connecticut, United States of America.
Background:
The role and mechanism of action of MIF in hyperoxia-induced acute lung injury (HALI) in the newborn lung are not known. We hypothesized that MIF is a critical regulatory molecule in HALI in the developing lung.
Methodology:
We studied newborn wild type (WT), MIF knockout (MIFKO), and MIF lung transgenic (MIFTG) mice in room air and hyperoxia exposure for 7 postnatal (PN) days. Lung morphometry was performed and mRNA and protein expression of vascular mediators were analyzed.
Results:
MIF mRNA and protein expression were significantly increased in WT lungs at PN7 of hyperoxia exposure. The pattern of expression of Angiopoietin 2 protein (in MIFKO>WT>MIFTG) was similar to the mortality pattern (MIFKO>WT>MIFTG) in hyperoxia at PN7. In room air, MIFKO and MIFTG had modest but significant increases in chord length, compared to WT. This was associated with decreased expression of Angiopoietin 1 and Tie 2 proteins in the MIFKO and MIFTG, as compared to the WT control lungs in room air. However, on hyperoxia exposure, while the chord length was increased from their respective room air controls, there were no differences between the 3 genotypes.
Conclusion:
These data point to the potential roles of Angiopoietins 1, 2 and their receptor Tie2 in the MIF-regulated response in room air and upon hyperoxia exposure in the neonatal lung.
Insights
Macrophage migration inhibitory factor (MIF) plays a role in neonatal lung injury from hyperoxia. Angiopoietins and Tie2 are involved in the MIF-regulated response to hyperoxia in developing lungs.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Molecular biology
Background:
- The role of Macrophage Migration Inhibitory Factor (MIF) in hyperoxia-induced acute lung injury (HALI) in newborns is unknown.
- MIF is hypothesized to be a critical regulator in HALI within the developing lung.
Purpose of the Study:
- To investigate the role and mechanism of MIF in neonatal HALI.
- To examine the relationship between MIF, Angiopoietins, and Tie2 in the neonatal lung under normoxia and hyperoxia.
Main Methods:
- Studied wild type (WT), MIF knockout (MIFKO), and MIF lung transgenic (MIFTG) newborn mice.
- Mice were exposed to room air or hyperoxia for 7 postnatal days.
- Analyzed lung morphometry and expression of vascular mediators (mRNA and protein).
Main Results:
- MIF expression increased in WT lungs with hyperoxia.
- Angiopoietin 2 expression correlated with mortality patterns in hyperoxia (MIFKO > WT > MIFTG).
- In normoxia, MIFKO and MIFTG showed altered lung structure and reduced Angiopoietin 1/Tie 2 expression compared to WT; these differences disappeared with hyperoxia.
Conclusions:
- Data suggest Angiopoietins 1, 2, and their receptor Tie2 are involved in the MIF-regulated response.
- These factors are implicated in both normoxic and hyperoxic conditions in the neonatal lung.
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