Apolipoprotein J / clusterin (apoJ) is a multifunctional glycoprotein up-regulated during various pathophysiological states and might represent a defence mechanism during cellular damage. An increase in either apoJ mRNA or protein expression is observed in numerous neurodegenerative conditions including Alzheimer’s disease, Parkinson’ disease, Pick disease, amyotrophic lateral sclerosis, and Huntington disease. Furthermore, these neurodegenerative disorders are characterized by intraneuronal abnormal filament accumulation associated with markers of oxidative injury. To determine whether apoJ is affected by oxidative stress, we evaluated the effects of oxidative insult on the expression of apoJ as part of a cellular response in viable human neuroblastoma IMR-32 cells. In our experimental model iron-ascorbate induced oxidative stress in IMR-32 cells without affecting cell viability, as detected by MTT-assay. It was found that IMR-32 cells express apoJ mature protein and that oxidative stress induced an up-regulation of apoJ level revealed by immunoblot analysis. The results of the present study suggest that an increase in apoJ expression may be a physiological defence able to reduce cell damage and maintain cell viability during periods of increased radical production. Supported by the University of Bologna, Funds for Selected Research Topics.
Dozza B., Zaccheo D., Strocchi P. (2005). NEURONAL APOLIPOPROTEIN J IS UP-REGULATED BY OXIDATIVE STRESS. s.l : s.n.
NEURONAL APOLIPOPROTEIN J IS UP-REGULATED BY OXIDATIVE STRESS
DOZZA, BARBARA;STROCCHI, PAOLA
2005
Abstract
Apolipoprotein J / clusterin (apoJ) is a multifunctional glycoprotein up-regulated during various pathophysiological states and might represent a defence mechanism during cellular damage. An increase in either apoJ mRNA or protein expression is observed in numerous neurodegenerative conditions including Alzheimer’s disease, Parkinson’ disease, Pick disease, amyotrophic lateral sclerosis, and Huntington disease. Furthermore, these neurodegenerative disorders are characterized by intraneuronal abnormal filament accumulation associated with markers of oxidative injury. To determine whether apoJ is affected by oxidative stress, we evaluated the effects of oxidative insult on the expression of apoJ as part of a cellular response in viable human neuroblastoma IMR-32 cells. In our experimental model iron-ascorbate induced oxidative stress in IMR-32 cells without affecting cell viability, as detected by MTT-assay. It was found that IMR-32 cells express apoJ mature protein and that oxidative stress induced an up-regulation of apoJ level revealed by immunoblot analysis. The results of the present study suggest that an increase in apoJ expression may be a physiological defence able to reduce cell damage and maintain cell viability during periods of increased radical production. Supported by the University of Bologna, Funds for Selected Research Topics.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
