ArticleEnvironmental health perspectives2011
Low-level gestational lead exposure increases retinal progenitor cell proliferation and rod photoreceptor and bipolar cell neurogenesis in mice.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Association of exposure to urinary and blood heavy metals with visual disability among U.S. adults in NHANES 2013-2018.Frontiers in public health · 2025Article
- Retinal toxicity of heavy metals and its involvement in retinal pathology.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2024Review
- Lead (Pb) Accumulation in Human THP-1 Monocytes/Macrophages In Vitro and the Influence on Cell Apoptosis.Biological trace element research · 2021Article
- Developmental exposure to PbChemosphere · 2020Article
- Late Effects ofFrontiers in behavioral neuroscience · 2020Article
- The cellular and compartmental profile of mouse retinal glycolysis, tricarboxylic acid cycle, oxidative phosphorylation, and ~P transferring kinases.Molecular vision · 2016Article
- Increased proliferation of late-born retinal progenitor cells by gestational lead exposure delays rod and bipolar cell differentiation.Molecular vision · 2016Article
- Dry eye modulates the expression of toll-like receptors on the ocular surface.Experimental eye research · 2015Article
- Lead exposure disrupts global DNA methylation in human embryonic stem cells and alters their neuronal differentiation.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Dynamics of the rhomboid-like protein RHBDD2 expression in mouse retina and involvement of its human ortholog in retinitis pigmentosa.The Journal of biological chemistry · 2013Article
- Developmental origins of adult diseases and neurotoxicity: epidemiological and experimental studies.Neurotoxicology · 2012Article
- Bcl-xL-mediated remodeling of rod and cone synaptic mitochondria after postnatal lead exposure: electron microscopy, tomography and oxygen consumption.Molecular vision · 2012Article
- Gestational lead exposure selectively decreases retinal dopamine amacrine cells and dopamine content in adult mice.Toxicology and applied pharmacology · 2011Article
- Redefining low lead levels.Environmental health perspectives · 2011Article
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Funding
Abstract
backgroundGestational lead exposure (GLE) produces novel and persistent rod-mediated electroretinographic (ERG) supernormality in children and adult animals.
objectivesWe used our murine GLE model to test the hypothesis that GLE increases the number of neurons in the rod signaling pathway and to determine the cellular mechanisms underlying the phenotype.
resultsBlood lead concentrations ([BPb]) in controls and after low-, moderate-, and high-dose GLE were ≤ 1, ≤ 10, approximately 25, and approximately 40 µg/dL, respectively, at the end of exposure [postnatal day 10 (PND10)]; by PND30 all [BPb] measures were ≤ 1 µg/dL. Epifluorescent, light, and confocal microscopy studies and Western blots demonstrated that late-born rod photoreceptors and rod and cone bipolar cells (BCs), but not Müller glial cells, increased in a nonmonotonic manner by 16-30% in PND60 GLE offspring. Retinal lamination and the rod:cone BC ratio were not altered. In vivo BrdU (5-bromo-2-deoxyuridine) pulse-labeling and Ki67 labeling of isolated cells from developing mice showed that GLE increased and prolonged retinal progenitor cell proliferation. TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) and confocal studies revealed that GLE did not alter developmental apoptosis or produce retinal injury. BrdU birth-dating and confocal studies confirmed the selective rod and BC increases and showed that the patterns of neurogenesis and gliogenesis were unaltered by GLE.
conclusionsOur findings suggest two spatiotemporal components mediated by dysregulation of different extrinsic/intrinsic factors: increased and prolonged cell proliferation and increased neuronal (but not glial) cell fate. These findings have relevance for neurotoxicology, pediatrics, public health, risk assessment, and retinal cell biology because they occurred at clinically relevant [BPb] and correspond with the ERG phenotype.
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