Induction of autophagy and autophagic cell @entity204 in damaged neural tissue after acute XXXX in @entity19 .

@entity66 @entity3145 @entity19 @entity22227 @entity1977 @entity1566 @entity204
STUDY DESIGN: Expression of light chain 3 ( @entity22227 ), a characteristic marker of autophagy, was examined by immunohistochemistry and Western blot using a @entity1566 ( @entity1566 ) model in @entity19 . Electron microscopic analysis was also performed to examine the anatomic formation of autophagy and autophagic cell @entity204 in the injured spinal cord. OBJECTIVE: To examine both biochemically and anatomically the activity of autophagy in the damaged neural tissue after @entity1566 . SUMMARY OF BACKGROUND DATA: Autophagy is the bulk degradation of intracellular proteins and organelles, and it is involved in a number of diseases. Autophagy can lead to nonapoptotic programmed cell @entity204 , which is called autophagic cell @entity204 . Recent researches have revealed the increased expression of @entity22227 and the anatomic formation of autophagy and autophagic cell @entity204 in damaged tissues of @entity66 models. However, previous studies have focused on apoptotic process but not autophagic activity as mechanism of @entity3145 after @entity1566 . To date, there has been no study to examine the expression of @entity22227 and the anatomic formation of autophagy after @entity1566 . METHODS: The spinal cord was hemitransected at T10 in adult female C57BL/6J @entity19 . The @entity22227 expression was examined by immunohistochemistry and Western blot. The anatomic formation of autophagic activity was investigated using electron microscopy. RESULTS: Immunohistochemistry showed that the number of the @entity22227 -positive cells significantly increased at the lesion site after hemisection. The increase of @entity22227 -positive cells was observed from 4 hours and peaked at 3 days, and it lasted for at least 21 days after hemisection. The @entity22227 -positive cells were observed in neurons, astrocytes, and oligodendrocytes. Western blot analysis demonstrated that the level of @entity22227 -II protein expression significantly increased in the injured spinal cord. Electron microscopy showed the formation of autophagic vacuoles to increase in the damaged cells. Furthermore, the nuclei in the transferase-mediated @entity1977 nick end labeling-positive cells expressed @entity22227 were round, which is consistent with autophagic cell @entity204 , and they were neither shrunken nor fragmented as is observed in apoptotic nuclei. CONCLUSION: This study suggested both biochemically and anatomically that autophagy was clearly activated and autophagic cell @entity204 was induced in the damaged neural tissue after @entity1566 .
