Dysregulation of Protein Kinase C in Adult Depression and Suicide: Evidence From Postmortem Brain Studies.
Int J Neuropsychopharmacol
; 24(5): 400-408, 2021 05 18.
Article
en En
| MEDLINE
| ID: mdl-33515455
BACKGROUND: Several lines of evidence suggest the abnormalities of protein kinase C (PKC) signaling system in mood disorders and suicide based primarily on the studies of PKC and its isozymes in the platelets and postmortem brain of depressed and suicidal subjects. In this study, we examined the role of PKC isozymes in depression and suicide. METHODS: We determined the protein and mRNA expression of various PKC isozymes in the prefrontal cortical region (Brodmann area 9) in 24 normal control subjects, 24 depressed suicide (DS) subjects, and 12 depressed nonsuicide (DNS) subjects. The levels of mRNA in the prefrontal cortex were determined by quantitative real-time reverse transcription PCR, and the protein expression was determined by western blotting. RESULTS: We observed a significant decrease in mRNA expression of PKCα, PKCßI, PKCδ, and PKCε and decreased protein expression in either the membrane or the cytosol fraction of PKC isozymes PKCα, PKCßI, PKCßII, and PKCδ in DS and DNS subjects compared with normal control subjects. CONCLUSIONS: The current study provides detailed evidence of specific dysregulation of certain PKC isozymes in the postmortem brain of DS and DNS subjects and further supports earlier evidence for the role of PKC in the platelets and brain of the adult and teenage depressed and suicidal population. This comprehensive study may lead to further knowledge of the involvement of PKC in the pathophysiology of depression and suicide.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteína Quinasa C
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Corteza Prefrontal
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Trastorno Depresivo Mayor
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Suicidio Completo
Límite:
Adult
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Int J Neuropsychopharmacol
Asunto de la revista:
NEUROLOGIA
/
PSICOFARMACOLOGIA
Año:
2021
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Reino Unido