Stress Response Caused by Chronic Alcohol Intake in Aged Rat Brain

Unno, Keiko; Asakura, Hiromi; Shibuya, Y; Kaihou, Masako; Fukatsu, Hideto; Okada, Shoji; Oku, Naoto

doi:10.1097/00000374-200207000-00012

Cited by 4 publications

(4 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The oxidative stress marker Hsp70 was demonstrated to have augmented release from neurons when exposed to HIV-1 with CD4-positive cell lines and macrophages (15,36,37). The results are also in agreement with other studies that have shown that EtOH can increase the expression of transcription factors (66) and the secretion of heat shock proteins in alcohol-exposed tissue (62,80,94).…”

Section: Coculturing Of Infected T Cells With Neurons or Neurons Exposupporting

confidence: 88%

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

Acheampong

Parveen

Mengistu

et al. 2007

J Virol

View full text Add to dashboard Cite

The AIDS-related dementia characterized by cognitive dysfunction, motor neuron disease, coordination abnormalities, and other neurological signs and symptoms develops in many human immunodeficiency virus type 1 (HIV-1)-infected individuals (17, 58). The molecular mechanisms involved in these HIV-1-associated dysfunctions of the central nervous system (CNS) remain incompletely explained and controversial (42,45). Studies have demonstrated that although the major reservoirs for productive infection within the CNS of HIV-1-infected individuals are microglia and monocytes/macrophages, infection of other CNSbased cell types, such as microvascular endothelial cells and neurons, also appears to occur (44,57,92). The role of lymphocytes in AIDS dementia has also been described previously (59,67,68). Of note, viral replication in cerebrospinal fluid is considered to be a marker for the severity of AIDS-related neurodegeneration (16,20). The CNS tissues are protected from the periphery by a structure known as blood-brain barrier (BBB), which limits the passage of solutes as well as infections into the brain (10). The tight junctions of brain microvascular endothelial cells strengthen the functional impermeability of BBB. Under certain pathological conditions, the BBB becomes compromised, providing access for infections/infected cells into the brain (64). The passage of HIV-1 entry into the brains of AIDS patients in vivo is not quite clear and is supposed to involve both free viruses and virally infected cells (4,89,91).HIV-1-infected individuals are under chronic oxidative stress, and antioxidants have proved to ameliorate infectionassociated oxidative stress. (81, 84). Oxidative stress involves

show abstract

Section: Coculturing Of Infected T Cells With Neurons or Neurons Exposupporting

confidence: 88%

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

Acheampong

Parveen

Mengistu

et al. 2007

J Virol

View full text Add to dashboard Cite

show abstract

“…Hsp70 participates in translation, protein translocation, proteolysis and protein folding, suppressing aggregation and reactivating denatured proteins [33]. When we exposed primary astrocyte cell cultures to ethanol, we observed a significant increase in Hsp70 content in the cells, supporting previous studies [13,34,35]. Interestingly, changes in the Hsp70 expression were smaller in those cells previously enriched with vit-C before being exposed to ethanol, indicating that cells were able to cope better with the ethanol-induced insult.…”

Section: Discussionsupporting

confidence: 85%

Protective effect of vitamin C against the ethanol mediated toxic effects on human brain glial cells

Sánchez‐Moreno

Paniagua

Madrid

et al. 2003

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

“…Other proteins, such as several HSP70s, showed an alcoholism‐induced shift from one isoform to another. Most HSP70 expression is stress‐induced 40, and different HSP70s are induced by short‐term 41–43 and long‐term 14, 15, 44, 45 alcohol consumption; however, some are also expressed at a basal level ( e.g . in human brain HSP70‐2 46, HSP70‐5 47 and HSP70‐8 48, 49).…”

Section: Discussionmentioning

confidence: 99%

Synaptic proteome changes in the superior frontal gyrus and occipital cortex of the alcoholic brain

Etheridge

Lewohl

Mayfield

et al. 2009

Proteomics Clinical Apps

View full text Add to dashboard Cite

Cognitive deficits and behavioral changes that result from chronic alcohol abuse are a consequence of neuropathological changes which alter signal transmission through the neural network. To focus on the changes that occur at the point of connection between the neural network cells, synaptosomal preparations from post-mortem human brain of six chronic alcoholics and six non-alcoholic controls were compared using 2D-DIGE. Functionally affected and spared regions (superior frontal gyrus, SFG, and occipital cortex, OC, respectively) were analyzed from both groups to further investigate the specific pathological response that alcoholism has on the brain. Forty-nine proteins were differentially regulated between the SFG of alcoholics and the SFG of controls and 94 proteins were regulated in the OC with an overlap of 23 proteins. Additionally, the SFG was compared to the OC within each group (alcoholics or controls) to identify region specific differences. A selection were identified by MALDI-TOF mass spectrometry revealing proteins involved in vesicle transport, metabolism, folding and trafficking, and signal transduction, all of which have the potential to influence synaptic activity. A number of proteins identified in this study have been previously related to alcoholism; however, the focus on synaptic proteins has also uncovered novel alcoholism-affected proteins. Further exploration of these proteins will illuminate the mechanisms altering synaptic plasticity, and thus neuronal signaling and response, in the alcoholic brain.

show abstract

Stress Response Caused by Chronic Alcohol Intake in Aged Rat Brain

Abstract: Chronic alcohol intake causes a stress response in the aged rat brain. It is thought that the increased level of Hsc70 is brought about by an increase of denatured proteins.

Cited by 4 publications

References 19 publications

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

Protective effect of vitamin C against the ethanol mediated toxic effects on human brain glial cells

Synaptic proteome changes in the superior frontal gyrus and occipital cortex of the alcoholic brain

Contact Info

Product

Resources

About