During postnatal heart valve development, glycosaminoglycan (GAG)-rich valve primordia transform into stratified valve leaflets composed of GAGs, fibrillar collagen, and elastin layers accompanied by decreased cell proliferation, as well as thinning and elongation. The neonatal period is characterized by the transition from a uterine environment to atmospheric oxygen, but the role of changing O2 levels in valve extracellular matrix (ECM) composition or morphogenesis are not well-characterized. Here, we show that tissue hypoxia decreases in mouse aortic valves in the days after birth, concomitant with ECM remodeling and cell cycle arrest of valve interstitial cells (VICs). The effects of hypoxia on late embryonic valve ECM composition, Sox9 expression, and cell proliferation were examined in chicken embryo aortic valve organ cultures. Maintenance of late embryonic chicken aortic valve organ cultures in a hypoxic environment promotes GAG expression, Sox9 nuclear localization, and indicators of hyaluronan (HA) remodeling, but does not affect fibrillar collagen content or cell proliferation. Chronic hypoxia also promotes GAG accumulation in murine adult heart valves in vivo. Together, these results support a role for hypoxia in maintaining a primitive GAG-rich matrix in developing heart valves prior to birth and also in induction of HA remodeling in adults.
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 December 2017.
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#24,763,244
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Outputs from American Journal of Physiology: Heart & Circulatory Physiology
#6,186
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Outputs of similar age from American Journal of Physiology: Heart & Circulatory Physiology
#53
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