Selective sensitivity of early postmitotic retinal cells to apoptosis induced by inhibition of protein synthesis.

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Title: Selective sensitivity of early postmitotic retinal cells to apoptosis induced by inhibition of protein synthesis.
Authors: Rehen, S. K. (AUTHOR), Neves, D. D. C. (AUTHOR), Fragel‐Madeira, L. (AUTHOR), Britto, L. R. G. (AUTHOR), Linden, R. (AUTHOR)
Source: European Journal of Neuroscience. Dec99, Vol. 11 Issue 12, p4349-4356. 8p. 1 Chart.
Subjects: Retina cytology, Apoptosis, Mitosis
Abstract: Abstract In previous work we showed that apoptosis in retinal tissue from developing rats can be induced by inhibition of protein synthesis (Rehen et al. 1996, Development, 122, 1439–1448). Here we show that recent postmitotic cells are the cells sensitive to apoptosis triggered by blockade of protein synthesis. To label all proliferating cells in the retina, a series of injections of the nucleotide analogue, bromo-deoxy-uridine (BrdU, 60 mg/kg b.w.), was given in rat pups. Then, explants of the retina were incubated in vitro with the inhibitor of protein synthesis anisomycin (1.0–3.2 μg/mL) for 1 day to induce apoptosis. Detection of apoptotic bodies under differential interference contrast microscopy was combined with immunocytochemistry for BrdU, proliferating cell nuclear antigen (PCNA) or for various markers of retinal cell differentiation. Despite the large number of BrdU- and PCNA-labelled cells in the tissue, the vast majority of the cells that underwent apoptosis were postmitotic cells which have left the mitotic cycle 3–4 days before. However, these cells were not labelled with antibodies to calretinin, calbindin, rhodopsin or to a Muller glial cell marker, suggesting that these are early postmitotic neurons. We suggest that during migration and initial differentiation, the apoptotic machinery is blocked by suppressor proteins, thus allowing recent postmitotic cells to find their final positions and differentiate while protected from apoptosis. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Selective sensitivity of early postmitotic retinal cells to apoptosis induced by inhibition of protein synthesis.
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  Data: <searchLink fieldCode="AR" term="%22Rehen%2C+S%2E+K%2E%22">Rehen, S. K.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Neves%2C+D%2E+D%2E+C%2E%22">Neves, D. D. C.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Fragel‐Madeira%2C+L%2E%22">Fragel‐Madeira, L.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Britto%2C+L%2E+R%2E+G%2E%22">Britto, L. R. G.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Linden%2C+R%2E%22">Linden, R.</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Dec99, Vol. 11 Issue 12, p4349-4356. 8p. 1 Chart.
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  Data: <searchLink fieldCode="DE" term="%22Retina+cytology%22">Retina cytology</searchLink><br /><searchLink fieldCode="DE" term="%22Apoptosis%22">Apoptosis</searchLink><br /><searchLink fieldCode="DE" term="%22Mitosis%22">Mitosis</searchLink>
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  Data: Abstract In previous work we showed that apoptosis in retinal tissue from developing rats can be induced by inhibition of protein synthesis (Rehen et al. 1996, Development, 122, 1439–1448). Here we show that recent postmitotic cells are the cells sensitive to apoptosis triggered by blockade of protein synthesis. To label all proliferating cells in the retina, a series of injections of the nucleotide analogue, bromo-deoxy-uridine (BrdU, 60 mg/kg b.w.), was given in rat pups. Then, explants of the retina were incubated in vitro with the inhibitor of protein synthesis anisomycin (1.0–3.2 μg/mL) for 1 day to induce apoptosis. Detection of apoptotic bodies under differential interference contrast microscopy was combined with immunocytochemistry for BrdU, proliferating cell nuclear antigen (PCNA) or for various markers of retinal cell differentiation. Despite the large number of BrdU- and PCNA-labelled cells in the tissue, the vast majority of the cells that underwent apoptosis were postmitotic cells which have left the mitotic cycle 3–4 days before. However, these cells were not labelled with antibodies to calretinin, calbindin, rhodopsin or to a Muller glial cell marker, suggesting that these are early postmitotic neurons. We suggest that during migration and initial differentiation, the apoptotic machinery is blocked by suppressor proteins, thus allowing recent postmitotic cells to find their final positions and differentiate while protected from apoptosis. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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        Value: 10.1046/j.1460-9568.1999.00868.x
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      – Code: eng
        Text: English
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      – SubjectFull: Retina cytology
        Type: general
      – SubjectFull: Apoptosis
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      – SubjectFull: Mitosis
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            NameFull: Britto, L. R. G.
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              M: 12
              Text: Dec99
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              Y: 1999
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