Neuron injury and apoptotic cell death in a mouse model of retinopathy of prematurity

Michael (Mike) Powers, J. P. Eubanks

Research output: Contribution to journalArticle

Abstract

Purpose. To evaluate retinal neurons for evidence of ischémie stress, morphologic alterations, and cell death in a mouse model of retinopathy of prematurity (ROP). Methods. Postnatal day 7 C57BL/6 mice were exposed to 75% O2 for 5 days (P12 O2) then recovered in room air for an additional 9 days (P21 O3). Tissue sections from paraffin-embedded hyperoxia-exposed mouse eyes as well as room air controls were examined on P12 & P21. Papanicolaou stain (EA 50) was used as a histological marker for ischémie neurons. Immunohistochemical staining for synaptophysin was used to examine the morphologic integrity of the neuron synapses. Apoptosis was detected in the retina using the TUNEL method. Results. Inner nuclear layer (INL) neurons were stained with EA 50 in the central retina (region of vaso-obl iteration) in the P12 02 eyes. EA 50 staining was not evident in the P21 O2 eyes or in control eyes. The plexiform layers were labeled for synaptophysin in the P12 & P21 control eyes. The P12 O2 eyes displayed irregular labelling along the outer plexiform layer (OPL) and cellular staining in the INL. The synaptophysin labeling was disrupted along the OPL in regions of retinal dysplasia in P21 O2 eyes. The P12 & P21 control eyes displayed a rare apoptotic retinal cell as determined by the TUNEL method. The P12 O2 eyes exhibited numerous stained cells in both nuclear layers in the central retina. The P21 O2 eyes exhibited an occasional stained neuron but significantly reduced from P12 O3. Conclusions. Oxygen-induced injury to the developing retina results in ischémie neurons, altered synaptic integrity and neuron cell death by apoptosis. Neuronal injury in the immature retina could contribute to subsequent photoreceptor dysfunction & altered visual function.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume38
Issue number4
StatePublished - 1997

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Retinopathy of Prematurity
Cell Death
Neurons
Wounds and Injuries
Retina
Synaptophysin
In Situ Nick-End Labeling
Staining and Labeling
Retinal Dysplasia
Air
Apoptosis
Retinal Neurons
Hyperoxia
Inbred C57BL Mouse
Paraffin
Synapses
Coloring Agents
Oxygen

ASJC Scopus subject areas

  • Ophthalmology

Cite this

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title = "Neuron injury and apoptotic cell death in a mouse model of retinopathy of prematurity",
abstract = "Purpose. To evaluate retinal neurons for evidence of isch{\'e}mie stress, morphologic alterations, and cell death in a mouse model of retinopathy of prematurity (ROP). Methods. Postnatal day 7 C57BL/6 mice were exposed to 75{\%} O2 for 5 days (P12 O2) then recovered in room air for an additional 9 days (P21 O3). Tissue sections from paraffin-embedded hyperoxia-exposed mouse eyes as well as room air controls were examined on P12 & P21. Papanicolaou stain (EA 50) was used as a histological marker for isch{\'e}mie neurons. Immunohistochemical staining for synaptophysin was used to examine the morphologic integrity of the neuron synapses. Apoptosis was detected in the retina using the TUNEL method. Results. Inner nuclear layer (INL) neurons were stained with EA 50 in the central retina (region of vaso-obl iteration) in the P12 02 eyes. EA 50 staining was not evident in the P21 O2 eyes or in control eyes. The plexiform layers were labeled for synaptophysin in the P12 & P21 control eyes. The P12 O2 eyes displayed irregular labelling along the outer plexiform layer (OPL) and cellular staining in the INL. The synaptophysin labeling was disrupted along the OPL in regions of retinal dysplasia in P21 O2 eyes. The P12 & P21 control eyes displayed a rare apoptotic retinal cell as determined by the TUNEL method. The P12 O2 eyes exhibited numerous stained cells in both nuclear layers in the central retina. The P21 O2 eyes exhibited an occasional stained neuron but significantly reduced from P12 O3. Conclusions. Oxygen-induced injury to the developing retina results in isch{\'e}mie neurons, altered synaptic integrity and neuron cell death by apoptosis. Neuronal injury in the immature retina could contribute to subsequent photoreceptor dysfunction & altered visual function.",
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T1 - Neuron injury and apoptotic cell death in a mouse model of retinopathy of prematurity

AU - Powers, Michael (Mike)

AU - Eubanks, J. P.

PY - 1997

Y1 - 1997

N2 - Purpose. To evaluate retinal neurons for evidence of ischémie stress, morphologic alterations, and cell death in a mouse model of retinopathy of prematurity (ROP). Methods. Postnatal day 7 C57BL/6 mice were exposed to 75% O2 for 5 days (P12 O2) then recovered in room air for an additional 9 days (P21 O3). Tissue sections from paraffin-embedded hyperoxia-exposed mouse eyes as well as room air controls were examined on P12 & P21. Papanicolaou stain (EA 50) was used as a histological marker for ischémie neurons. Immunohistochemical staining for synaptophysin was used to examine the morphologic integrity of the neuron synapses. Apoptosis was detected in the retina using the TUNEL method. Results. Inner nuclear layer (INL) neurons were stained with EA 50 in the central retina (region of vaso-obl iteration) in the P12 02 eyes. EA 50 staining was not evident in the P21 O2 eyes or in control eyes. The plexiform layers were labeled for synaptophysin in the P12 & P21 control eyes. The P12 O2 eyes displayed irregular labelling along the outer plexiform layer (OPL) and cellular staining in the INL. The synaptophysin labeling was disrupted along the OPL in regions of retinal dysplasia in P21 O2 eyes. The P12 & P21 control eyes displayed a rare apoptotic retinal cell as determined by the TUNEL method. The P12 O2 eyes exhibited numerous stained cells in both nuclear layers in the central retina. The P21 O2 eyes exhibited an occasional stained neuron but significantly reduced from P12 O3. Conclusions. Oxygen-induced injury to the developing retina results in ischémie neurons, altered synaptic integrity and neuron cell death by apoptosis. Neuronal injury in the immature retina could contribute to subsequent photoreceptor dysfunction & altered visual function.

AB - Purpose. To evaluate retinal neurons for evidence of ischémie stress, morphologic alterations, and cell death in a mouse model of retinopathy of prematurity (ROP). Methods. Postnatal day 7 C57BL/6 mice were exposed to 75% O2 for 5 days (P12 O2) then recovered in room air for an additional 9 days (P21 O3). Tissue sections from paraffin-embedded hyperoxia-exposed mouse eyes as well as room air controls were examined on P12 & P21. Papanicolaou stain (EA 50) was used as a histological marker for ischémie neurons. Immunohistochemical staining for synaptophysin was used to examine the morphologic integrity of the neuron synapses. Apoptosis was detected in the retina using the TUNEL method. Results. Inner nuclear layer (INL) neurons were stained with EA 50 in the central retina (region of vaso-obl iteration) in the P12 02 eyes. EA 50 staining was not evident in the P21 O2 eyes or in control eyes. The plexiform layers were labeled for synaptophysin in the P12 & P21 control eyes. The P12 O2 eyes displayed irregular labelling along the outer plexiform layer (OPL) and cellular staining in the INL. The synaptophysin labeling was disrupted along the OPL in regions of retinal dysplasia in P21 O2 eyes. The P12 & P21 control eyes displayed a rare apoptotic retinal cell as determined by the TUNEL method. The P12 O2 eyes exhibited numerous stained cells in both nuclear layers in the central retina. The P21 O2 eyes exhibited an occasional stained neuron but significantly reduced from P12 O3. Conclusions. Oxygen-induced injury to the developing retina results in ischémie neurons, altered synaptic integrity and neuron cell death by apoptosis. Neuronal injury in the immature retina could contribute to subsequent photoreceptor dysfunction & altered visual function.

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