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Titolo:
CLOSTRIDIUM-DIFFICILE TOXIN-B ACTIVATES CALCIUM INFLUX REQUIRED FOR ACTIN DISASSEMBLY DURING CYTOTOXICITY
Autore:
GILBERT RJ; POTHOULAKIS C; LAMONT JT; YAKUBOVICH M;
Indirizzi:
ST ELIZABETHS MED CTR,280 WASHINGTON ST BOSTON MA 02135 ST ELIZABETHS HOSP BOSTON,DIV GASTROENTEROL BOSTON MA 02315 ST ELIZABETHS HOSP BOSTON,DEPT BIOMED RES BOSTON MA 02315 TUFTS UNIV,SCH MED BOSTON MA 02315 BOSTON UNIV HOSP,DIV GASTROENTEROL BOSTON MA 02118 BOSTON UNIV,SCH MED BOSTON MA 02118
Titolo Testata:
American journal of physiology: Gastrointestinal and liver physiology
fascicolo: 3, volume: 31, anno: 1995,
pagine: 487 - 495
SICI:
0193-1857(1995)31:3<487:CTACIR>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTESTINAL SMOOTH-MUSCLE; INTRACELLULAR CALCIUM; CHOLERA-TOXIN; RABBIT ILEUM; A GENE; CELLS; INCREASES; PERMEABILITY; MONOLAYERS; EXPRESSION;
Keywords:
CALCIUM; CYTOTOXICITY; ACTIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
40
Recensione:
Indirizzi per estratti:
Citazione:
R.J. Gilbert et al., "CLOSTRIDIUM-DIFFICILE TOXIN-B ACTIVATES CALCIUM INFLUX REQUIRED FOR ACTIN DISASSEMBLY DURING CYTOTOXICITY", American journal of physiology: Gastrointestinal and liver physiology, 31(3), 1995, pp. 487-495

Abstract

The principal cellular response to Clostridium difficile toxin B, a protein toxin associated with antibiotic-associated colitis, is the disassembly of actin microfilaments. Although receptor-activated signal transduction mechanisms have been proposed to mediate these effects, the intracellular events that precede actin breakdown are unknown. In NIH-3T3 fibroblasts, toxin B induced an elevation of intracellular calcium possessing either a slow (minutes) or fast (seconds) rise time, followed by a sustained elevation of calcium concentration. Subcellular analysis of steady-state calcium distribution after toxin B demonstrated that the increase of calcium was homogeneous throughout the cytosol and did not vary based on the kinetics of the initial calcium rise. Ahcalcium responses were blocked by substitution with calcium-free buffer or buffer containing lanthanum chloride, indicating that the rise in calcium was attributable to calcium influx from the extracellular space. Quantitatively similar responses were observed in primary cultured gastric smooth muscle and AR42J pancreatic tumor cells, suggesting that toxin-induced calcium signal transduction was conserved between cell types. The morphological response to toxin B consisted of sequential dissociation of the actin cytoskeleton from membrane attachments, retraction of actin stress fibers from the periphery to the perinuclear region, loss of fiber alignment, and cell rounding. The actin reorganization associated with term B was blocked by incubation of cells in calcium-free media or the clamping of intracellular calcium with cell-permeant calcium chelating agents. These results demonstrate that the calcium influx activated by C. difficile toxin B is a necessary condition for the breakdown of filamentous actin associated with cytotoxicity.

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Documento generato il 02/04/20 alle ore 02:20:26