Abstract
BackgroundWe have previously shown that vitamin D deficiency has a detrimental impact on lung development. In this study, we aimed to identify the mechanisms linking vitamin D with lung development using a mouse model of dietary manipulation.MethodsFemale offspring were euthanized at different time-points; embryonic day (E)14.5, E17.5 or postnatal day (P)7. Lung tissue was collected for mass spectrometry-based proteomic analysis. Label-free quantitation was used to identify the differentially expressed proteins and ELISA confirmed the expression of selected proteins. Lungs from separate groups of mice were fixed and processed for stereological assessment of lung structure.ResultsNo differences in protein expression between vitamin D deficient and replete mice were detected at E14.5 and E17.5, whereas 66 proteins were differentially expressed in P7 lungs. The expression of pulmonary surfactant-associated protein B (SP-B) and peroxiredoxin 5 (PRDX5) were reduced in P7 lungs of vitamin D deficient mice, while the production of collagen type Ι alpha 1 (COL1A1) was higher in lungs of vitamin D deficient mice. There were no differences in lung volume, parenchymal volume, volume of airspaces or surface area of airspaces between vitamin D deficient and vitamin D replete mice across three time-points.ConclusionsThe difference in protein expression during the early postnatal time-point suggests that vitamin D deficiency may induce alterations of lung structure and function in later life during alveolarization stage through impaired pulmonary surfactant production and anti-oxidative stress ability as well as enhanced collagen synthesis. These data provided a plausible mechanism linking maternal vitamin D deficiency with altered postnatal lung function.
Highlights
We have previously shown that vitamin D deficiency has a detrimental impact on lung development
Differential protein expression In line with the Principal components analysis (PCA), no significant differences in protein expression between lungs of vitamin D deficient and replete mice were detected at E14.5 or E17.5 (n = 6/ group)
Based on proteins that were detected in all samples, there were 8 proteins with increased expression and 29 proteins with decreased expression in vitamin D deficient P7 lungs compared to vitamin D replete lungs (Fig. 3a)
Summary
We have previously shown that vitamin D deficiency has a detrimental impact on lung development. A plethora of studies have shown cross-sectional associations between vitamin D deficiency and chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis [3,4,5]. These associations are confounded by the effect of chronic disease on physical activity levels [6] which are highly correlated with sun exposure and, vitamin D synthesis [7]. While clinical studies have shown no benefit of vitamin D supplementation in established disease, other studies have suggested that vitamin D deficiency may be a precursor to the development of respiratory disease [12]. Genomic analyses of lung tissue from mice and humans have identified a
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