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Difructose anhydride III and sodium caprate activate paracellular transport via different intracellular events in Caco-2 cells.
Life Sci. 2006 Jun 20; 79(4):401-10.LS

Abstract

A nondigestible disaccharide, difructose anhydride (DFA) III, is known to activate calcium transport via tight junctions (TJs); however, the characteristics of and mechanisms for the increase in paracellular transport induced by DFAIII have not been clarified. We compared the effect of DFAIII with that of sodium caprate (C10), a well-known enhancer of TJ permeability, on the changes in TJ proteins, transport of paracellular markers, and effects of nine cellular signaling blockers using Caco-2 monolayers. The addition of DFAIII (0-100mmol/L) and C10 (0-10mmol/L) to the apical medium of the Caco-2 monolayers dose-dependently decreased transepithelial electrical resistance (TER), which is an indicator of TJ permeability. The reduction with C10 was much faster than that with DFAIII. Transport of the paracellular markers of various molecular weights (182-43,200) was elevated by the addition of 100mmol/L DFAIII and 10mmol/L C10. The transport rates were much in the presence of C10 than of DFAIII, while the reduction in TER by two treatments was similar (from 1000 to 300Omega cm(2)). Treatment with DFAIII and C10 changed the distribution of actin filament and claudin-1, but not occludin, junctional adhesion molecule-1, or zonula occludens-1; however, alterations in the patterns of the TJ proteins differed according to treatment. An inhibitor of myosin light chain kinase and a chelator of intracellular calcium ion ([Ca(2+)](i)) attenuated the TER reduction by C10, but not by DFAIII. These data demonstrate that the increase in TJ permeability induced by DFAIII results from the alterations to actin and claudin-1 via [Ca(2+)](i)-independent mechanisms.

Authors+Show Affiliations

Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kita-ku, Sapporo 060-8589, Japan.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16566947

Citation

Suzuki, Takuya, and Hiroshi Hara. "Difructose Anhydride III and Sodium Caprate Activate Paracellular Transport Via Different Intracellular Events in Caco-2 Cells." Life Sciences, vol. 79, no. 4, 2006, pp. 401-10.
Suzuki T, Hara H. Difructose anhydride III and sodium caprate activate paracellular transport via different intracellular events in Caco-2 cells. Life Sci. 2006;79(4):401-10.
Suzuki, T., & Hara, H. (2006). Difructose anhydride III and sodium caprate activate paracellular transport via different intracellular events in Caco-2 cells. Life Sciences, 79(4), 401-10.
Suzuki T, Hara H. Difructose Anhydride III and Sodium Caprate Activate Paracellular Transport Via Different Intracellular Events in Caco-2 Cells. Life Sci. 2006 Jun 20;79(4):401-10. PubMed PMID: 16566947.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Difructose anhydride III and sodium caprate activate paracellular transport via different intracellular events in Caco-2 cells. AU - Suzuki,Takuya, AU - Hara,Hiroshi, Y1 - 2006/03/29/ PY - 2005/06/03/received PY - 2005/12/17/revised PY - 2006/01/16/accepted PY - 2006/3/29/pubmed PY - 2006/7/13/medline PY - 2006/3/29/entrez SP - 401 EP - 10 JF - Life sciences JO - Life Sci VL - 79 IS - 4 N2 - A nondigestible disaccharide, difructose anhydride (DFA) III, is known to activate calcium transport via tight junctions (TJs); however, the characteristics of and mechanisms for the increase in paracellular transport induced by DFAIII have not been clarified. We compared the effect of DFAIII with that of sodium caprate (C10), a well-known enhancer of TJ permeability, on the changes in TJ proteins, transport of paracellular markers, and effects of nine cellular signaling blockers using Caco-2 monolayers. The addition of DFAIII (0-100mmol/L) and C10 (0-10mmol/L) to the apical medium of the Caco-2 monolayers dose-dependently decreased transepithelial electrical resistance (TER), which is an indicator of TJ permeability. The reduction with C10 was much faster than that with DFAIII. Transport of the paracellular markers of various molecular weights (182-43,200) was elevated by the addition of 100mmol/L DFAIII and 10mmol/L C10. The transport rates were much in the presence of C10 than of DFAIII, while the reduction in TER by two treatments was similar (from 1000 to 300Omega cm(2)). Treatment with DFAIII and C10 changed the distribution of actin filament and claudin-1, but not occludin, junctional adhesion molecule-1, or zonula occludens-1; however, alterations in the patterns of the TJ proteins differed according to treatment. An inhibitor of myosin light chain kinase and a chelator of intracellular calcium ion ([Ca(2+)](i)) attenuated the TER reduction by C10, but not by DFAIII. These data demonstrate that the increase in TJ permeability induced by DFAIII results from the alterations to actin and claudin-1 via [Ca(2+)](i)-independent mechanisms. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/16566947/Difructose_anhydride_III_and_sodium_caprate_activate_paracellular_transport_via_different_intracellular_events_in_Caco_2_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(06)00100-7 DB - PRIME DP - Unbound Medicine ER -