Prenatal Vitamin A Deficiency May Contribute to Asthma
Murine study shows altered phenotype persists postnatally, regardless of adult vitamin A status
THURSDAY, Feb. 20, 2014 (HealthDay News) -- Early fetal retinoic acid (RA) deficiency is associated with altered airway smooth muscle phenotype, with RA restricting airway smooth muscle differentiation, according to an experimental study published in the Feb. 3 issue of the Journal of Clinical Investigation.
Felicia Chen, M.D., from the Boston University School of Medicine, and colleagues examined the impact of early fetal bioactive vitamin A metabolite RA deficiency on postnatal lung structure and function. The authors note that increasing evidence suggests that vitamin A deficiency in utero correlates with abnormal airway smooth muscle function in postnatal life.
The researchers found that, during airway formation, endogenous RA plays a key role in restricting the airway smooth muscle cell differentiation program. Based on murine models of pharmacologic, genetic, and dietary vitamin A/RA deficiency, there was a consistent association observed between disruption of RA signaling during embryonic development and alteration of airway smooth muscle phenotype, with markedly increased smooth muscle marker expression. Regardless of the adult vitamin A status, the aberrant phenotype persisted, manifesting as structural changes in the bronchial smooth muscle and airway hyperresponsiveness, with no indication of inflammation.
"Our data reveal a role for endogenous RA signaling in restricting smooth muscle differentiation and preventing precocious and excessive smooth muscle differentiation when airways are forming," the authors write.