Actin cytoskeleton role in the structural response of epithelial (MDCK) cells to low extracellular Ca2+

Citation
E. Frixione et al., Actin cytoskeleton role in the structural response of epithelial (MDCK) cells to low extracellular Ca2+, J MUSCLE R, 22(3), 2001, pp. 229-242
Citations number
37
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY
ISSN journal
0142-4319 → ACNP
Volume
22
Issue
3
Year of publication
2001
Pages
229 - 242
Database
ISI
SICI code
0142-4319(2001)22:3<229:ACRITS>2.0.ZU;2-B
Abstract
Kinetic and stereometric assessment of the mechanical responses of epitheli al cells to variations in the concentration of extracellular Ca2+ was carri ed out in vivo at the single cell level. Continuous monitoring of individua l MDCK cells in subconfluent cultures attested to an intense, immediately r elaxable, and cytochalasin D-sensitive contraction, equivalent to that seen in confluent monolayers following depletion of external Ca2+ (<0.1 mM). In creasingly greater and less readily reversible contractions were performed upon repeated stimulation with short-term cycles of alternating normal (30 min) and low Ca2+ (30 min) media. Constriction of a narrow horizontal girdl e corresponding in position to the major ring-like bundle of actin filament s eventually develops into a deep lateral furrow in intensely contracted ce lls. Substantial membrane infolding in the contracted state is indicated al so by stereometric estimates of apparent bounding surface area. Irrespectiv e of the contracted or relaxed cell condition, rhodamine-phalloidin labelin g showed a marginal position of the ring-like bundle of microfilaments and other components of the actin cytoskeleton. These results suggest, contrary to prevalent views, that the actin-myosin system stays associated to the c ortex and retains contractile capability in epithelial cells deprived of ex ternal Ca2+. Hence, the mechanical responses to variations of Ca2+ may be a n overstrained expression of a physiological mechanism.