(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 February 3 issue of the Journal of Clinical Investigation.

Felicia Chen, MD, 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.

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