Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells.

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Abstract Text:

Toru Iizaka,Mayumi Tsuji,Hideto Oyamada,Yuri Morio,Katsuji Oguchi,Toru Iizaka,Mayumi Tsuji,Hideto Oyamada,Yuri Morio,Katsuji Oguchi,Toru Iizaka,Mayumi Tsuji,Hideto Oyamada,Yuri Morio,Katsuji Oguchi,

The accumulation of hydrophobic bile acid, such as glycochenodeoxycholic acid (GCDCA), in the liver has been thought to induce hepatocellular damage in human chronic cholestatic liver diseases. We previously reported that GCDCA-induced apoptosis was promoted by both mitochondria-mediated and endoplasmic reticulum (ER) stress-associated pathways in rat hepatocytes. In this study, we elucidated the relationship between these pathways in GCDCA-induced apoptotic HepG2 cells. HepG2 cells were treated with GCDCA (100-500muM) with or without a caspase-8 inhibitor, Z-IETD-fluoromethyl ketone (Z-IETD-FMK) (30muM) for 3-24h. We demonstrated the presence of both apoptotic pathways in these cells; that is, we showed increases in cleaved caspase-3 proteins, the release of cytochrome c from mitochondria, and the expression of ER resident molecular chaperone Bip mRNA and ER stress response-associated transcription factor Chop mRNA. On the other hand, pretreatment with Z-IETD-FMK significantly reduced the increases, compared with treatment with GCDCA alone. Immunofluorescence microscopic analysis showed that treatment with GCDCA increased the cleavage of BAP31, an integral membrane protein of ER, and pretreatment with Z-IETD-FMK suppressed the increase of caspase-8 and BAP31 cleavage. In conclusion, these results suggest that intact activated caspase-8 may promote and amplify the ER stress response by cleaving BAP31 in GCDCA-induced apoptotic cells.

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Publishing Authors By Initials

T Iizaka,M Tsuji,H Oyamada,Y Morio,K Oguchi,T Iizaka,M Tsuji,H Oyamada,Y Morio,K Oguchi,T Iizaka,M Tsuji,H Oyamada,Y Morio,K Oguchi,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Toxicology

VOLUME: 241

Page Numbers: 146-56

Journal Abbreviation: Toxicology

ISSN: 0300-483X

DAY: 5

MONTH: 09

YEAR: 2007

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 361055

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells.

AFFILIATION: Department of Pharmacology, School of Medicine, Showa University, Hatanodai 1-5-8, Shinagawa-ku, Tokyo 142-8555, Japan.

Country: Ireland

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Toxicology

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells Related Publications

• A multicenter phase II study of local radiation therapy for stage IEA mucosa-associated lymphoid tissue lymphomas: a preliminary report from the Japan Radiation Oncology Group (JAROG).
• Detection of human papillomavirus infection in squamous tumours of the conjunctiva and lacrimal sac by immunohistochemistry, in situ hybridisation, and polymerase chain reaction.
• Effects of pioglitazone on increases in visceral fat accumulation and oxidative stress in spontaneously hypertensive hyperlipidemic rats fed a high-fat diet and sucrose solution.
• Evidence based quality management of the clinical formulations: determination of the expiration date of the powdered medicine prepared by grinding tablets.
• Formulation study of intravesical oxybutynin instillation solution with enhanced retention in bladder.
• Glyceraldehyde-3-phosphate dehydrogenases from human erythrocytes.
• Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells.
• Internal iliac artery aneurysm rupture with aorto-enteric fistula after reconstruction of abdominal aortic aneurysm: report of a case.
• Matrix metalloproteinase-9 in spontaneously hypertensive hyperlipidemic rats.
• ON-pathway disturbance in two siblings.
• Oral vitamin C supplementation in hemodialysis patients and its effect on the plasma level of oxidized ascorbic acid and Cu/Zn superoxide dismutase, an oxidative stress marker.
• Scanning laser Doppler flowmeter study of retinal blood flow in macular area of healthy volunteers.