Zhonghua er bi yan hou ke za zhi · 2001
[Expression of bcl-2 in facial motoneurons and its ultrastructural localization following facial nerve injury].
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Dai C, Huang X, Zhao H, Wang Z, Li K
Аннотация
OBJECTIVE: To explore the expression of bcl-2 in facial motoneurons and its subcellular distribution.
METHODS: Wistar rats were used in this study. Facial nerve transection was performed at stylomastoid foramen or internal acoustic meatus. Facial nerve crush was made at stylomastiod foramen. The animal survived for 1, 3, 7, 15, 30 and 60 days respectively. Facial nucleus was treated with bcl-2 monoclonal antibody or bcl-2 DIG-labelling probe and studied with immunohistochemistry and in situ hybridization. The bcl-2 positive motoneuron was investigated with immuno-electron microscope.
RESULTS: It was demonstrated that bcl-2 protein level was corresponded with bcl-2 mRNA expression. The level of bcl-2 expression in facial motoneurons was high in normal facial nerve. It increased on the first day and declined on the third day post-transection in facial motoneuron. It reached the lowest level on the 15th days following facial nerve injury (P < 0.05). The expression recovered to normal level in two months (P > 0.05). After facial nerve transected, the reduction of bcl-2 expression was more significant when facial nerve transected close to facial nucleus than that far from facial nucleus (P < 0.05). Comparing to facial nerve transection in stylomastoid foramen, there was more intensive bcl-2 expression following facial nerve crush (P < 0.05). Further study showed that bcl-2 primarily resided in the nuclear envelop, endoplasmic reticulum and mitochondrial membrane.
CONCLUSIONS: These data indicated that high level bcl-2 protein may prevent facial motoneuron death following facial nerve injury. It is suggested that overexpression bcl-2 by transgene may prevent facial motoneurons death.
METHODS: Wistar rats were used in this study. Facial nerve transection was performed at stylomastoid foramen or internal acoustic meatus. Facial nerve crush was made at stylomastiod foramen. The animal survived for 1, 3, 7, 15, 30 and 60 days respectively. Facial nucleus was treated with bcl-2 monoclonal antibody or bcl-2 DIG-labelling probe and studied with immunohistochemistry and in situ hybridization. The bcl-2 positive motoneuron was investigated with immuno-electron microscope.
RESULTS: It was demonstrated that bcl-2 protein level was corresponded with bcl-2 mRNA expression. The level of bcl-2 expression in facial motoneurons was high in normal facial nerve. It increased on the first day and declined on the third day post-transection in facial motoneuron. It reached the lowest level on the 15th days following facial nerve injury (P < 0.05). The expression recovered to normal level in two months (P > 0.05). After facial nerve transected, the reduction of bcl-2 expression was more significant when facial nerve transected close to facial nucleus than that far from facial nucleus (P < 0.05). Comparing to facial nerve transection in stylomastoid foramen, there was more intensive bcl-2 expression following facial nerve crush (P < 0.05). Further study showed that bcl-2 primarily resided in the nuclear envelop, endoplasmic reticulum and mitochondrial membrane.
CONCLUSIONS: These data indicated that high level bcl-2 protein may prevent facial motoneuron death following facial nerve injury. It is suggested that overexpression bcl-2 by transgene may prevent facial motoneurons death.