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A unique role for the nonmuscle myosin IIA in regulation of epithelial apical junctions
Author(s) -
Ivanov Andrei I,
Bachar Moshe,
Babbin Brian,
Adelstein Robert S,
Nusrat Asma,
Parkos Charles A
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a763-c
Subject(s) - adherens junction , microbiology and biotechnology , tight junction , extracellular , gene isoform , chemistry , biology , cell , cadherin , biochemistry , gene
The integrity of epithelial monolayers depends on the formation of tight junctions (TJ) and adherens junctions (AJ). TJ and AJ associate with underlying actomyosin bundles that are critical for their biogenesis and functions. We investigated roles of three nonmuscle myosin II (NMM II) isoforms, A, B, and C in the regulation of epithelial TJ and AJ. NMM IIA, NMM IIB and NMM IIC were all expressed in SK‐CO15 and Caco‐2 colonic epithelial cell lines, and all isoforms colocalized with perijunctional F‐actin. Using isoform‐specific siRNAs, we selectively down‐regulated expression of the NMM IIA, NMM IIB, or NMM IIC in SK‐CO15 cells. Down‐regulation of the NMM IIA caused the following morphological and functional changes: transformation from an orthogonal epithelial to a protrusive fibroblast‐like cell shape; a three fold decrease in transepithelial electrical resistance; attenuation of TJ and AJ disassembly and cell contraction induced by extracellular calcium depletion; inhibition of TJ and AJ reassembly after calcium repletion. None of the above changes were observed after down‐regulation of either the NMM IIB or NMM IIC. These findings suggest that the NMM IIA plays a unique role in regulation of the dynamics and barrier properties of epithelial apical junctions. Supported by the Crohn’s and Colitis Foundation of America (AII) and NIH (AN and CAP).