Title
Calyculin a Causes Endothelial Monolayer Barrier Failure Without Stress Fiber Formation
Document Type
Article
Publication Date
12-1-1996
Description
Calyculin A (CA, 5 nM), a scrine-threonme phosphatase inhibitor, has been reported to induce large hole formation between adjacent bovine pulmonary artery endothelial cells (BPAEC) by a contractile mechanism similar to that produced by thromhin (AJP 269:L99-L108. 1995). We tested this contraction hypothesis by measuring BPAFC monolayer barrier function (AJP 264:111798-1809. 1993) before and alter CA (1-20 nM I addition, then stained filamentous (F)-actin with rhodamine-phalloidm. CA (5 nM) caused large holes to form across BPAEC monolayers within I hr. Dense peripheral bands of F-actin and occasional stress fibers were seen by fluorescence microscopy in control BPAHCs. C'A (5 nM) caused reversible large hole (>l-20 urn radius) formation in monolayers without increased stress fiber formation. CA caused cell rounding with punctate F-actin at the cell edged and within the cytoplasm of spread cells. These data do not support the contraction hypothesis of CA-induced endothelial barrier failure. Rather, they suggest that CA-induced endothelial barrier failure may be associated with loss of cell-cell and cell-substiate adhesion.
Citation Information
Schaeffer, R. C.; Klein, J. D.; O'Neill, W. C.; Diwan, A. M.; Sirada, S. J.; and Thompson, W. J.. 1996. Calyculin a Causes Endothelial Monolayer Barrier Failure Without Stress Fiber Formation. FASEB Journal. Vol.10(3). ISSN: 0892-6638