Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy.

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Abstract Text:

The relationship between the degradative process of autophagy and cellular death pathways remains unclear. Macroautophagy may potentially function to prevent or promote cell death, and both effects have been reported in studies of cells with a block in macroautophagy. To better delineate the function of macroautophagy in cell death, we contrasted the responses to death stimuli in wild-type and atg5(-/-) murine embryonic fibroblasts. We have reported that a knockout of the critical macroautophagy gene ATG5 sensitizes cells to death receptor ligand-induced death from Fas and tumor necrosis factor-alpha. Death occurs by caspase-dependent apoptosis resulting from activation of the mitochondrial death pathway. In contrast, atg5(-/-) cells are more resistant to death induced by oxidative stress from menadione or UV light. This resistance was associated with an upregulation of chaperone-mediated autophagy. Inhibition of this form of autophagy sensitizes cells to death from menadione, suggesting that the compensatory upregulation of chaperone-mediated autophagy, and not the loss of macroautophagy, prevents death from menadione. These findings demonstrate that the effects of a loss of macroautophagy on the cellular death response differ depending on the mechanism of cellular injury and the compensatory changes in other forms of autophagy.

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Publishing Authors By Initials

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE: 2008 Jul-Aug

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Autophagy

VOLUME: 4

Page Numbers: 516-8

Journal Abbreviation: Autophagy

ISSN: 1554-8635

DAY: 27

MONTH: 02

YEAR: 2008

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101265188

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy.

AFFILIATION: Department of Medicine and the Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: DK044234

ACRONYM: DK

MEDLINETA: Autophagy

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy Related Publications

• A prospective investigation of major depressive disorder and comorbidity in abused and neglected children grown up.
• Age differences in life satisfaction as a function of discrepancy between real and ideal self concepts.
• Autoimmune liver disease.
• CNS lymphomatoid granulomatosis in AIDS: CT and MR appearances.
• Cell signaling in oxidative stress-induced liver injury.
• Clinical features, differential diagnosis and treatment of autoimmune hepatitis in the elderly.
• Compensatory mechanisms and the type of injury determine the fate of cells with impaired macroautophagy.
• Employment opportunities for older adults: engineering design and research issues.
• Features associated with treatment failure in type 1 autoimmune hepatitis and predictive value of the model of end-stage liver disease.
• Frequency, behavior, and prognostic implications of antimitochondrial antibodies in type 1 autoimmune hepatitis.
• Genetic factors affecting the occurrence, clinical phenotype, and outcome of autoimmune hepatitis.
• HLA DQ gene dosage and risk and severity of celiac disease.
• Loss of macroautophagy promotes or prevents fibroblast apoptosis depending on the death stimulus.
• Predictive factors for hepatocellular carcinoma in type 1 autoimmune hepatitis.
• Regulation of hepatocyte apoptosis by oxidative stress.
• Safety issues in the management of autoimmune hepatitis.
• The cost-effectiveness of a behavior intervention with caregivers of patients with Alzheimer's disease.
• [Binge eating and obesity in children]
• [Statistical analysis of some size parameters of haversian systems in femoral, ground transverse sections in man and animals (author's transl)]