Document Detail

Dynamin is involved in human epithelial cell vacuolation caused by the Helicobacter pylori-produced cytotoxin VacA.
MedLine Citation:
PMID:  11160160     Owner:  NLM     Status:  MEDLINE    
The Helicobacter pylori-produced cytotoxin VacA induces intracellular vacuolation. To elucidate the molecular mechanism of vacuole formation by VacA, we examined the participation of dynamin, a GTPase functioning in intracellular vesicle formation, in human HeLa cells. Immunocytochemistry revealed that endogenous dynamin was localized to vacuoles induced by VacA. In cells transiently transfected with a GTPase-defective (dominant-negative) dynamin mutant, VacA failed to induce vacuolation. In contrast, VacA did induce vacuolation in cells transiently transfected with wild-type dynamin. Furthermore, under VacA treatment, neutral red dye uptake, a parameter of VacA-induced vacuolation, was inhibited in cells stably transfected with the dominant-negative dynamin mutant. In contrast, uptake was markedly enhanced in cells stably transfected with wild-type dynamin. Moreover, VacA cytopathic effects on the viability of HeLa cells were inhibited in cells stably transfected with dominant-negative dynamin-1. Sequential immunocytochemical observation confirmed that expression of dominant-negative dynamin did not affect VacA attachment to or internalization into HeLa cells. We suggest that dynamin is involved in the intracellular vacuolation induced by VacA.
J Suzuki; H Ohnsihi; H Shibata; A Wada; T Hirayama; T Iiri; N Ueda; C Kanamaru; T Tsuchida; H Mashima; H Yasuda; T Fujita
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  107     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2001 Feb 
Date Detail:
Created Date:  2001-02-22     Completed Date:  2001-03-08     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  363-70     Citation Subset:  AIM; IM    
Department of Internal Medicine, University of Tokyo School of Medicine, Tokyo, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Bacterial Proteins / antagonists & inhibitors,  biosynthesis*
Cell Survival
Cytotoxins / biosynthesis*
Duodenal Diseases / microbiology
Dynamin I
Epithelial Cells / metabolism*
Fluorescent Antibody Technique
GTP Phosphohydrolases / genetics,  metabolism*
Hela Cells
Helicobacter pylori / metabolism*
Reg. No./Substance:
0/Bacterial Proteins; 0/Cytotoxins; 0/VacA protein, Helicobacter pylori; EC I; EC 3.6.1.-/GTP Phosphohydrolases; EC

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

Previous Document:  Inhibition of STAT3 signaling leads to apoptosis of leukemic large granular lymphocytes and decrease...
Next Document:  Glucocorticoids upregulate CD40 ligand expression and induce CD40L-dependent immunoglobulin isotype ...