Tiny toes. Tiny fingers. Tiny diapers. The word “tiny” almost perfectly describes infants born very prematurely. Yet, it fails to properly describe the battle for survival these tiny warriors endure. And the more premature the baby, the harder the fight. Can recent advances in medicine help boost the odds in the warriors’ favor?

Upon entering the world, preemies struggle to breathe with underdeveloped lungs. Medical intervention in the form of oxygen therapy or mechanical ventilation can help, but many babies receiving such treatments often develop bronchopulmonary dysplasia (BPD) (Baker, Abman, & Mourani, 2014). This disease is characterized by problems with the development of the veins and arteries that feed into and out of lungs and air sacs. Not too surprisingly, BPD can give rise to more conditions, such as pulmonary vascular disease (PVD) or pulmonary hypertension, which in turn significantly increase infant mortality. Diagnosing these conditions can be difficult, but a better understanding of their molecular underpinnings may help identify the tiny warriors at greatest risk early enough to intervene successfully.

Researchers are answering the call to battle. Using an arsenal of scientific methodologies (including the proteomic analysis of blood samples from premature infants), one group found that current medical interventions can cause a decrease in levels of a critical protein called “platelet-derived growth factor receptor a” (PDGF-Ra) (Oak et al., 2017). Decreasing the amount of PDGF-Ra experimentally in animal models leads to the manifestation of traits similar to those seen in BPD-afflicted infants. The same researchers also found that adding back PDGF-Ra could rescue the observed consequences of the simulated medical intervention, suggesting a new way to attack the diseases that arise from standard treatments.

In another answer to the call-of-action, a different group used proteomics to better understand how PVD arises (Wagner et al., 2018). In the results, it was not too surprising to see proteins associated with the PDGF signalling network on the list of potential biomarkers. Surprisingly, some of the other biomarker candidates suggest new signaling pathways may be involved in the onset of PVD. Although exciting, future work is needed not only to confirm, but also expand upon these early suggestive findings.

With each answer to the call to battle, we are moving ever closer to improving the odds for the tiny warriors. The day may soon come when these tiny ones no longer struggle for breath or suffer the unintended consequences of the medical community’s life-saving interventions. When it does come, it will truly be a happy victory.

 

References

Baker, C. D., Abman, S. H., & Mourani, P. M. (2014). Pulmonary Hypertension in Preterm Infants with Bronchopulmonary Dysplasia. Pediatr Allergy Immunol Pulmonol, 27(1), 8-16. doi:10.1089/ped.2013.0323

Oak, P., Pritzke, T., Thiel, I., Koschlig, M., Mous, D. S., Windhorst, A., . . . Hilgendorff, A. (2017). Attenuated PDGF signaling drives alveolar and microvascular defects in neonatal chronic lung disease. EMBO Mol Med, 9(11), 1504-1520. doi:10.15252/emmm.201607308

Wagner, B. D., Babinec, A. E., Carpenter, C., Gonzalez, S., O’Brien, G., Rollock, K., . . . Abman, S. H. (2018). Proteomic Profiles Associated with Early Echocardiogram Evidence of Pulmonary Vascular Disease in Preterm Infants. Am J Respir Crit Care Med, 197(3), 394-397. doi:10.1164/rccm.201703-0654LE