ArticleFrontiers in ophthalmology2022
Markers of Hypoxia and Metabolism Correlate With Cell Differentiation in Retina and Lens Development.
Article in Frontiers in ophthalmology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Sigma 1 Receptor Activation Coordinates Metabolic Stress Responses to Protect Retinal Vasculature in Ischemic Retinopathy.Investigative ophthalmology & visual science · 2026Article
- The 3D Genome Structure of a Blcap-Linked Silencer Loop Regulates Terminal Differentiation During Lens Fiber Cell Denucleation.Investigative ophthalmology & visual science · 2025Article
- Modulating mitochondrial metabolism: a neuroprotective mechanism for hypoxic-ischemic preconditioning.Cell regeneration (London, England) · 2025Review
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4 authors.
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Abstract
Recent studies have provided novel insights of co-development of the neural and vascular elements of the retina. Knowledge of these relationships are crucial to understand the impact of therapeutic measures in Retinopathy of Prematurity (ROP). ROP is imposed by therapeutic oxygen upon immature retinal blood vessels and neural cells causing delayed development and vascular regression. However, the impact of hyperoxia on developing retinal neurons is less understood because some aspects of normal development remain unknown. The metabolic changes during differentiation of retinal progenitor cells to functional neurons is one such aspect. We correlated immunomarkers of hypoxia with markers of metabolic change in developing retinal neurons during the early postnatal period in mice. The same marker proteins were studied in secondary lens fiber differentiation at postnatal day-3 (P3). Nuclear localization of the oxygen-sensitive subunits of hypoxia inducible factor, HIF-1α and HIF-2α was correlated with increasing mitochondrial content in differentiating neurons. Nuclear HIF was also correlated with AMP-dependent protein kinase (AMPK), and the AMPK phosphorylation target PPAR-gamma coactivator-1alpha (PGC-1α), the principal regulator of mitochondrial biogenesis. Expression of AMPK, PGC1α and HIF-2α in secondary fiber differentiation was visible in each profile of the lens equator. Strong nuclear localization for all markers was present at the onset of secondary fiber differentiation, and reflected changes in size, mitochondrial content, and metabolism. We speculate that the 'physiological hypoxia' that drives retinal vascular development is cell-specific and reliant upon neuronal differentiation and mitochondrial biogenesis. We suggest that the onset of differentiation increases energy consumption that is detected by AMPK. In turn AMPK increases mitochondrial biogenesis
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