ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Bim expression indicates the pathway to retinal cell death in development and degeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting circular RNA-Glra2 alleviates retinal neurodegeneration induced by ocular hypertension.Aging · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Bim Expression Modulates Branching Morphogenesis of the Epithelium and Endothelium.Biomolecules · 2022Article
- All-Trans Retinoic Acid Attenuates Blue Light-Induced Apoptosis of Retinal Photoreceptors by Upregulating MKP-1 Expression.Molecular neurobiology · 2021Article
- Mouse Retinal Organoid Growth and Maintenance in Longer-Term Culture.Frontiers in cell and developmental biology · 2021Article
- IER3IP1 deficiency leads to increased β-cell death and decreased β-cell proliferation.Oncotarget · 2017Article
- General pathophysiology in retinal degeneration.Developments in ophthalmology · 2014Review
- Article
- Photoreceptor cell death and rescue in retinal detachment and degenerations.Progress in retinal and eye research · 2013Review
- Prolonged expression of Puma in cholinergic amacrine cells during the development of rat retina.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Article
- The Bcl-2 family member BIM has multiple glaucoma-relevant functions in DBA/2J mice.Scientific reports · 2012Article
- Article
- BBC3 (PUMA) regulates developmental apoptosis but not axonal injury induced death in the retina.Molecular neurodegeneration · 2011Article
- Bim is responsible for the inherent sensitivity of the developing retinal vasculature to hyperoxia.Developmental biology · 2011Article
- Ionic dysregulatory phenotyping of pathologic retinal thinning with manganese-enhanced MRI.Investigative ophthalmology & visual science · 2008Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death (PCD) during development of the mouse retina involves activation of the mitochondrial pathway. Previous work has shown that the multidomain Bcl-2 family proteins Bax and Bak are fundamentally involved in this process. To induce mitochondrial membrane permeabilization, Bax and Bak require that prosurvival members of the family be inactivated by binding of "BH3-only" members. We showed previously that the BH3-only protein BimEL is highly expressed during postnatal retinal development but decreases dramatically thereafter. The purpose of this study was to investigate a possible role for Bim, in retinal development and degeneration, upstream of Bax and Bak. Bim-/- mice analyzed for defective retinal development exhibit an increase in retinal thickness and a delay in PCD, thereby confirming a role for Bim. We also demonstrate that in response to certain death stimuli, bim+/+ retinal explants upregulate BimEL leading to caspase activation and cell death, whereas bim-/- explants are resistant to apoptosis. Finally, we analyzed Bim expression in the retinal degeneration (rd) mouse, an in vivo model of retinal degeneration. Bim isoforms, which decrease during development, are not reexpressed during retinal degeneration and ultimately photoreceptor cells die by a caspase-independent mechanism. Thus, we conclude that in cases in which BimEL is reexpressed during pathological cell death, developmental cell death pathways are reactivated. However, the absence of BimEL expression correlates with caspase-independent death in the rd model.
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