Changing sensitivity to cell death during development of retinal photoreceptors

Photoreceptor cell death occurs during both normal and pathological retinal development. We tested for selective induction and blockade of cell death in either retinal photoreceptors or their precursors. Organotypical retinal explants from rats at postnatal days 3–11 were treated in vitro for 24 hr...

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Published inJournal of neuroscience research Vol. 74; no. 6; pp. 875 - 883
Main Authors Chiarini, Luciana B., Leal-Ferreira, Mona Lisa, de Freitas, Fabíola G., Linden, Rafael
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 15.12.2003
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Abstract Photoreceptor cell death occurs during both normal and pathological retinal development. We tested for selective induction and blockade of cell death in either retinal photoreceptors or their precursors. Organotypical retinal explants from rats at postnatal days 3–11 were treated in vitro for 24 hr with thapsigargin, okadaic acid, etoposide, anisomycin, or forskolin. Explant sections were examined for cell death, and identification of either photoreceptors or proliferating/immediate postmitotic cells followed imunohistochemistry for either rhodopsin or bromodeoxyuridine and proliferating cell nuclear antigen, respectively. Photoreceptor cell death was selectively induced by either thapsigargin or okadaic acid, whereas death of proliferating/immediate postmitotic cells was induced by etoposide. Prelabeling of proliferating precursors allowed direct demonstration of changing sensitivity of photoreceptors to various chemicals. Degeneration of both photoreceptors and proliferating/immediate postmitotic cells depended on protein synthesis. Increase of intracellular cyclic AMP blocked degeneration of postmitotic, but not of proliferating, photoreceptor precursors. The selective induction and blockade of cell death show that developing photoreceptors undergo progressive changes in mechanisms of programmed cell death associated with phenotypic differentiation. © 2003 Wiley‐Liss, Inc.
AbstractList Photoreceptor cell death occurs during both normal and pathological retinal development. We tested for selective induction and blockade of cell death in either retinal photoreceptors or their precursors. Organotypical retinal explants from rats at postnatal days 3-11 were treated in vitro for 24 hr with thapsigargin, okadaic acid, etoposide, anisomycin, or forskolin. Explant sections were examined for cell death, and identification of either photoreceptors or proliferating/immediate postmitotic cells followed imunohistochemistry for either rhodopsin or bromodeoxyuridine and proliferating cell nuclear antigen, respectively. Photoreceptor cell death was selectively induced by either thapsigargin or okadaic acid, whereas death of proliferating/immediate postmitotic cells was induced by etoposide. Prelabeling of proliferating precursors allowed direct demonstration of changing sensitivity of photoreceptors to various chemicals. Degeneration of both photoreceptors and proliferating/immediate postmitotic cells depended on protein synthesis. Increase of intracellular cyclic AMP blocked degeneration of postmitotic, but not of proliferating, photoreceptor precursors. The selective induction and blockade of cell death show that developing photoreceptors undergo progressive changes in mechanisms of programmed cell death associated with phenotypic differentiation.
Photoreceptor cell death occurs during both normal and pathological retinal development. We tested for selective induction and blockade of cell death in either retinal photoreceptors or their precursors. Organotypical retinal explants from rats at postnatal days 3–11 were treated in vitro for 24 hr with thapsigargin, okadaic acid, etoposide, anisomycin, or forskolin. Explant sections were examined for cell death, and identification of either photoreceptors or proliferating/immediate postmitotic cells followed imunohistochemistry for either rhodopsin or bromodeoxyuridine and proliferating cell nuclear antigen, respectively. Photoreceptor cell death was selectively induced by either thapsigargin or okadaic acid, whereas death of proliferating/immediate postmitotic cells was induced by etoposide. Prelabeling of proliferating precursors allowed direct demonstration of changing sensitivity of photoreceptors to various chemicals. Degeneration of both photoreceptors and proliferating/immediate postmitotic cells depended on protein synthesis. Increase of intracellular cyclic AMP blocked degeneration of postmitotic, but not of proliferating, photoreceptor precursors. The selective induction and blockade of cell death show that developing photoreceptors undergo progressive changes in mechanisms of programmed cell death associated with phenotypic differentiation. © 2003 Wiley‐Liss, Inc.
Author Linden, Rafael
Chiarini, Luciana B.
Leal-Ferreira, Mona Lisa
de Freitas, Fabíola G.
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Snippet Photoreceptor cell death occurs during both normal and pathological retinal development. We tested for selective induction and blockade of cell death in either...
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SubjectTerms Animals
apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Cell Death - drug effects
Cell Death - physiology
cell differentiation
Cell Differentiation - drug effects
Cell Differentiation - physiology
cell proliferation
Cells, Cultured
Okadaic Acid - pharmacology
Photoreceptor Cells - cytology
Photoreceptor Cells - drug effects
Photoreceptor Cells - growth & development
Rats
retinal degeneration
rods
Title Changing sensitivity to cell death during development of retinal photoreceptors
URI https://api.istex.fr/ark:/67375/WNG-PNGGJLXT-W/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjnr.10739
https://www.ncbi.nlm.nih.gov/pubmed/14648592
https://search.proquest.com/docview/19186039
Volume 74
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