Phalloidin enhances endothelial barrier function and reduces inflammatory permeability in vitro

Microvasc Res. 1988 May;35(3):308-15. doi: 10.1016/0026-2862(88)90085-4.

Abstract

Phalloidin, a potent microfilament toxin, induces polymerization of actin in vitro and in vivo. In a permeability assay, bovine aortic endothelial cell cultured on microcarrier beads exclude significantly more serum albumin after 30 min treatment with 10(-6), 10(-8), and 10(-10) M phalloidin than controls. Furthermore, pretreatment of microcarriers with 10(-8) M phalloidin significantly reduces permeability increases by histamine, bradykinin, thromboxane A2 mimetic, and cytochalasin B, (all at 10(-6) M). Phalloidin also causes significant surface area and perimeter increases in cultured endothelial cells. The cells also display increased acting stress fibers and show a weblike cytoskeletal pattern of microfilaments. These data suggest that in vitro the endothelial junctional barrier may be enhanced in part by assembly of actin filaments.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Aorta, Abdominal
  • Bradykinin / pharmacology
  • Cattle
  • Cell Membrane Permeability / drug effects*
  • Cells, Cultured
  • Cytochalasin B / pharmacology
  • Cytoskeleton / drug effects*
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / ultrastructure
  • Histamine / pharmacology
  • Microspheres
  • Oligopeptides / pharmacology*
  • Phalloidine / pharmacology*
  • Thromboxane A2 / pharmacology

Substances

  • Oligopeptides
  • Phalloidine
  • Cytochalasin B
  • Thromboxane A2
  • Histamine
  • Bradykinin