Markers of Hypoxia and Metabolism Correlate With Cell Differentiation in Retina and Lens Development

Recent studies have provided novel insights of co-development the neural and vascular elements retina. Knowledge these relationships are crucial to understand impact therapeutic measures in Retinopathy Prematurity (ROP). ROP is imposed by oxygen upon immature retinal blood vessels cells causing delayed development regression. However, hyperoxia on developing neurons less understood because some aspects normal remain unknown. The metabolic changes during differentiation progenitor functional one such aspect. We correlated immunomarkers hypoxia with markers change early postnatal period mice. same marker proteins were studied secondary lens fiber at day-3 (P3). Nuclear localization oxygen-sensitive subunits inducible factor, HIF-1α HIF-2α was increasing mitochondrial content differentiating neurons. HIF also AMP-dependent protein kinase (AMPK), AMPK phosphorylation target PPAR-gamma coactivator-1alpha (PGC-1α), principal regulator biogenesis. Expression AMPK, PGC1α visible each profile equator. Strong nuclear for all present onset differentiation, reflected size, content, metabolism. speculate that ‘physiological hypoxia’ drives cell-specific reliant neuronal suggest increases energy consumption detected AMPK. In turn biogenesis via PGC-1α. Mitochondrial may then create intracellular activates HIF. This progression congruent expression HIF-2α. retina defined than as it involve remnant from embryonic sustained increased caused consumption. first report involvement HIF-2α, PGC-1α development.