Differential activation of proapoptotic molecules between mouse and rat models of distal motor trigeminal denervation

Shiori Harada, Satoshi O. Suzuki, Yoshihiro Seki, Seiji Nakamura, Toru Iwaki

Research output: Contribution to journalArticle

Abstract

Background: We previously developed a rat trigeminal motor neuron axotomy model involving masseter and temporal muscle resection to study pathological changes of the central nucleus after peripheral nerve injury caused by oral surgery. Because motor neurons are reported to be more vulnerable to axotomy in mice than rats, we compared the degeneration process of the trigeminal motor nucleus in the rat model with a similar mouse model. Methods: We removed masseter and temporal muscles of adult mice or rats. Animals were sacrificed at 3, 7, 14, 28, 42, and 56days post-operation, and the trigeminal motor nuclei were histologically analyzed. Results: Size reduction, but no neuronal loss, was seen in the trigeminal motor nuclei in both mice and rats. Time-dependent Noxa expression, starting at 1week post-operation (wpo), was seen in the mouse model. By 8wpo, mice expressed a higher level of Noxa than rats. Additionally, we noted persistent expression of cleaved caspase-3 in mice but not in rats. Conversely, apoptosis-inducing factor (AIF), which executes DNA fragmentation in the nucleus, was not translocated to the nucleus in either model. Conclusions: Our findings indicate differential activation of motor neuron apoptosis pathways after axotomy in mice and rats. Lack of activation of caspase-independent pathways and distal end denervation in our model might be related to the survival of motor neurons after axonal injury. These findings could be relevant to future neuroprotective strategies for peripheral nerve injury caused by oral surgeries.

Original languageEnglish
Pages (from-to)354-360
Number of pages7
JournalJournal of Oral Pathology and Medicine
Volume41
Issue number4
DOIs
Publication statusPublished - Apr 1 2012

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Denervation
Motor Neurons
Axotomy
Noxae
Temporal Muscle
Masseter Muscle
Peripheral Nerve Injuries
Oral Surgery
Apoptosis Inducing Factor
DNA Fragmentation
Caspases
Apoptosis
Wounds and Injuries
Trigeminal Motor Nucleus

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Oral Surgery
  • Otorhinolaryngology
  • Cancer Research
  • Periodontics

Cite this

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title = "Differential activation of proapoptotic molecules between mouse and rat models of distal motor trigeminal denervation",
abstract = "Background: We previously developed a rat trigeminal motor neuron axotomy model involving masseter and temporal muscle resection to study pathological changes of the central nucleus after peripheral nerve injury caused by oral surgery. Because motor neurons are reported to be more vulnerable to axotomy in mice than rats, we compared the degeneration process of the trigeminal motor nucleus in the rat model with a similar mouse model. Methods: We removed masseter and temporal muscles of adult mice or rats. Animals were sacrificed at 3, 7, 14, 28, 42, and 56days post-operation, and the trigeminal motor nuclei were histologically analyzed. Results: Size reduction, but no neuronal loss, was seen in the trigeminal motor nuclei in both mice and rats. Time-dependent Noxa expression, starting at 1week post-operation (wpo), was seen in the mouse model. By 8wpo, mice expressed a higher level of Noxa than rats. Additionally, we noted persistent expression of cleaved caspase-3 in mice but not in rats. Conversely, apoptosis-inducing factor (AIF), which executes DNA fragmentation in the nucleus, was not translocated to the nucleus in either model. Conclusions: Our findings indicate differential activation of motor neuron apoptosis pathways after axotomy in mice and rats. Lack of activation of caspase-independent pathways and distal end denervation in our model might be related to the survival of motor neurons after axonal injury. These findings could be relevant to future neuroprotective strategies for peripheral nerve injury caused by oral surgeries.",
author = "Shiori Harada and Suzuki, {Satoshi O.} and Yoshihiro Seki and Seiji Nakamura and Toru Iwaki",
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T1 - Differential activation of proapoptotic molecules between mouse and rat models of distal motor trigeminal denervation

AU - Harada, Shiori

AU - Suzuki, Satoshi O.

AU - Seki, Yoshihiro

AU - Nakamura, Seiji

AU - Iwaki, Toru

PY - 2012/4/1

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N2 - Background: We previously developed a rat trigeminal motor neuron axotomy model involving masseter and temporal muscle resection to study pathological changes of the central nucleus after peripheral nerve injury caused by oral surgery. Because motor neurons are reported to be more vulnerable to axotomy in mice than rats, we compared the degeneration process of the trigeminal motor nucleus in the rat model with a similar mouse model. Methods: We removed masseter and temporal muscles of adult mice or rats. Animals were sacrificed at 3, 7, 14, 28, 42, and 56days post-operation, and the trigeminal motor nuclei were histologically analyzed. Results: Size reduction, but no neuronal loss, was seen in the trigeminal motor nuclei in both mice and rats. Time-dependent Noxa expression, starting at 1week post-operation (wpo), was seen in the mouse model. By 8wpo, mice expressed a higher level of Noxa than rats. Additionally, we noted persistent expression of cleaved caspase-3 in mice but not in rats. Conversely, apoptosis-inducing factor (AIF), which executes DNA fragmentation in the nucleus, was not translocated to the nucleus in either model. Conclusions: Our findings indicate differential activation of motor neuron apoptosis pathways after axotomy in mice and rats. Lack of activation of caspase-independent pathways and distal end denervation in our model might be related to the survival of motor neurons after axonal injury. These findings could be relevant to future neuroprotective strategies for peripheral nerve injury caused by oral surgeries.

AB - Background: We previously developed a rat trigeminal motor neuron axotomy model involving masseter and temporal muscle resection to study pathological changes of the central nucleus after peripheral nerve injury caused by oral surgery. Because motor neurons are reported to be more vulnerable to axotomy in mice than rats, we compared the degeneration process of the trigeminal motor nucleus in the rat model with a similar mouse model. Methods: We removed masseter and temporal muscles of adult mice or rats. Animals were sacrificed at 3, 7, 14, 28, 42, and 56days post-operation, and the trigeminal motor nuclei were histologically analyzed. Results: Size reduction, but no neuronal loss, was seen in the trigeminal motor nuclei in both mice and rats. Time-dependent Noxa expression, starting at 1week post-operation (wpo), was seen in the mouse model. By 8wpo, mice expressed a higher level of Noxa than rats. Additionally, we noted persistent expression of cleaved caspase-3 in mice but not in rats. Conversely, apoptosis-inducing factor (AIF), which executes DNA fragmentation in the nucleus, was not translocated to the nucleus in either model. Conclusions: Our findings indicate differential activation of motor neuron apoptosis pathways after axotomy in mice and rats. Lack of activation of caspase-independent pathways and distal end denervation in our model might be related to the survival of motor neurons after axonal injury. These findings could be relevant to future neuroprotective strategies for peripheral nerve injury caused by oral surgeries.

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