Document Detail


The regulatory mechanism of 4-phenylbutyric acid against ER stress-induced autophagy in human gingival fibroblasts.
MedLine Citation:
PMID:  22864750     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Endoplasmic reticulum (ER) stress is closely connected to autophagy. When cells are exposed to ER stress, cells exhibit enhanced protein degradation and form autophagosomes. In this study, we demonstrate that the chemical chaperone, 4-phenylbutyric acid (4-PBA), regulates ER stressinduced cell death and autophagy in human gingival fibroblasts. We found that 4-PBA protected cells against thapsigargin-induced apoptotic cell death but did not affect the reduced cell proliferation. ER stress induced by thapsigargin was alleviated by 4-PBA through the regulation of several ER stress-inducible, unfolded protein response related proteins including GRP78, GRP94, C/EBP homologous protein, phospho-eIF-2α, eIF-2α, phospho-JNK1 (p46) and phospho-JNK2/3 (p54), JNK1, IRE-1α, PERK, and sXBP-1. Compared with cells treated with thapsigargin alone, cells treated with both 4-PBA and thapsigargin showed lower levels of Beclin-1, LC-3II and autophagic vacuoles, indicating that 4-PBA also inhibited autophagy induced by ER stress. This study suggests that 4-PBA may be a potential therapeutic agent against ER stress-associated pathologic situations.
Authors:
Do-Sung Kim; Bo Li; Ki Yon Rhew; Hyo-Won Oh; Hyun-Dae Lim; Wan Lee; Han-Jung Chae; Hyung-Ryong Kim
Publication Detail:
Type:  Journal Article     Date:  2012-08-03
Journal Detail:
Title:  Archives of pharmacal research     Volume:  35     ISSN:  0253-6269     ISO Abbreviation:  Arch. Pharm. Res.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-08-06     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8000036     Medline TA:  Arch Pharm Res     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  1269-78     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Institute of Cardiovascular Research, School of Medicine, Chonbuk National University, Jeonju, Chonbuk, 561-180, Korea.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  The effects of ginsenoside Rb1 on JNK in oxidative injury in cardiomyocytes.
Next Document:  Attenuation of scopolamine-induced cognitive dysfunction by obovatol.