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Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase.
Am J Physiol Gastrointest Liver Physiol. 2000 Nov; 279(5):G875-85.AJ

Abstract

The intracellular mechanisms that mediate cytochalasin-induced increase in intestinal epithelial tight junction (TJ) permeability are unclear. In this study, we examined the involvement of myosin light chain kinase (MLCK) in this process, using the filter-grown Caco-2 intestinal epithelial monolayers. Cytochalasin B (Cyto B) (5 microg/ml) produced an increase in Caco-2 MLCK activity, which correlated with the increase in Caco-2 TJ permeability. The inhibition of Cyto B-induced MLCK activation prevented the increase in Caco-2 TJ permeability. Additionally, myosin-Mg(2+)-ATPase inhibitor and metabolic inhibitors (which inhibit MLCK induced actin-myosin contraction) also prevented the Cyto B-induced increase in Caco-2 TJ permeability. Cyto B caused a late-phase (15-30 min) aggregation of actin fragments into large actin clumps, which was also inhibited by MLCK inhibitors. Cyto B produced a morphological disturbance of the ZO-1 TJ proteins, visually correlating with the functional increase in Caco-2 TJ permeability. The MLCK and myosin-Mg(2+)-ATPase inhibitors prevented both the functional increase in TJ permeability and disruption of ZO-1 proteins. These findings suggested that Cyto B-induced increase in Caco-2 TJ permeability is regulated by MLCK activation.

Authors+Show Affiliations

Division of Gastroenterology, Department of Medicine, Department of Veterans Affairs Medical Center, California State University, Long Beach 90822, California. tyma@uci.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

11052983

Citation

Ma, T Y., et al. "Cytochalasin B Modulation of Caco-2 Tight Junction Barrier: Role of Myosin Light Chain Kinase." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 279, no. 5, 2000, pp. G875-85.
Ma TY, Hoa NT, Tran DD, et al. Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase. Am J Physiol Gastrointest Liver Physiol. 2000;279(5):G875-85.
Ma, T. Y., Hoa, N. T., Tran, D. D., Bui, V., Pedram, A., Mills, S., & Merryfield, M. (2000). Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase. American Journal of Physiology. Gastrointestinal and Liver Physiology, 279(5), G875-85.
Ma TY, et al. Cytochalasin B Modulation of Caco-2 Tight Junction Barrier: Role of Myosin Light Chain Kinase. Am J Physiol Gastrointest Liver Physiol. 2000;279(5):G875-85. PubMed PMID: 11052983.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase. AU - Ma,T Y, AU - Hoa,N T, AU - Tran,D D, AU - Bui,V, AU - Pedram,A, AU - Mills,S, AU - Merryfield,M, PY - 2000/10/29/pubmed PY - 2001/2/28/medline PY - 2000/10/29/entrez SP - G875 EP - 85 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 279 IS - 5 N2 - The intracellular mechanisms that mediate cytochalasin-induced increase in intestinal epithelial tight junction (TJ) permeability are unclear. In this study, we examined the involvement of myosin light chain kinase (MLCK) in this process, using the filter-grown Caco-2 intestinal epithelial monolayers. Cytochalasin B (Cyto B) (5 microg/ml) produced an increase in Caco-2 MLCK activity, which correlated with the increase in Caco-2 TJ permeability. The inhibition of Cyto B-induced MLCK activation prevented the increase in Caco-2 TJ permeability. Additionally, myosin-Mg(2+)-ATPase inhibitor and metabolic inhibitors (which inhibit MLCK induced actin-myosin contraction) also prevented the Cyto B-induced increase in Caco-2 TJ permeability. Cyto B caused a late-phase (15-30 min) aggregation of actin fragments into large actin clumps, which was also inhibited by MLCK inhibitors. Cyto B produced a morphological disturbance of the ZO-1 TJ proteins, visually correlating with the functional increase in Caco-2 TJ permeability. The MLCK and myosin-Mg(2+)-ATPase inhibitors prevented both the functional increase in TJ permeability and disruption of ZO-1 proteins. These findings suggested that Cyto B-induced increase in Caco-2 TJ permeability is regulated by MLCK activation. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/11052983/Cytochalasin_B_modulation_of_Caco_2_tight_junction_barrier:_role_of_myosin_light_chain_kinase_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.2000.279.5.G875?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -