Microfilamentous system and secretion of enzyme in the exocrine pancreas. Effect of cytochalasin B.

Abstract

The microfilaments in the acinar cell of the exocrine pancreas are essentially located in the apical part of the cell: thin microfilaments (50 A), cytochalasin B (CB)-sensitive, form the axis of the microvilli and a network lying beneath the apical membrane; thicker filaments (100 A), at least partly CB-insensitive, form bundles parallel to the plasma cell membrane and the desmosomal links. CB interaction with the acinar cell of the exocrine pancreas involves at least two sites: a membrane site involved in the inhibitory effect of CB on the monosaccharide transport and a less sensitive site at the filamentous level at least partly responsible for the inhibitory effect of CB in the secretion of the exportable enzyme from the pancreatic cell. CB did not alter the energy balance of the acinar cell nor the exchanges of 45Ca between the extracellular medium and the pancreatic tissue. CB (2 x 10 -7 and 2 x 10 -6 M) has secretagogue properties whereas CB (2 • 10 -s M) has inhibitory effect on stimulated secretion and secretagogue properties. The mechanism of these secretory effects is not yet explained. The analysis presented in this investigation affords strong evidence for the involvement of the microfilamentous network in the last steps of the secretory cycle in the acinar cell of the exocrine pancreas.

Effect of glucagon on digestive enzyme synthesis, transport and secretion in mouse pancreatic acinar cells.

“…Cytochalasin B distorted the luminal membrane structure resulting in disappearance of microfilaments underlying the apical plasma membrane and loss of apical microvilli (Williams, 1977). It has been hypothesized (Case, 1978), that CB may cause a nonvisible disruption of microfilaments associated with impairment of glucose carrier mechanism (Bauduin, Stock, Vincent & Grenier, 1975). In the present study, glucagon-stimulated amylase secretion was inhibited by cytochalasin B to the same extent as bethanechol and CCK-PZ-stimulated amylase secretion indicating that structural integrity of luminal membrane is important in glucagon mediated secretion.…”

Surface dynamics in living acinar cells imaged by atomic force microscopy: Identification of plasma membrane structures involved in exocytosis

“…Earlier studies by Bauduin et al (37) demonstrated that high concentrations of cytochalasin B inhibit secretion from the exocrine pancreas. Previous studies in pancreatic acinar cells and other cell types also demonstrated a requirement for actin filaments in exocytosis (37)(38)(39)(40)(41). A recent study by Muallem et al (42) further demonstrates this role of actin and implicates its participation at a late step of exocytosis in the exocrine pancreas.…”

Actin coating of secretory granules during regulated exocytosis correlates with the release of rab3D

“…The rareness of the ACG phenomenon is reminiscent of the low frequency at which exocytotic events are observed at the ultrastructural level and suggests that ACGs are very rapidly formed and transient structures. This also explains why, up to now, ACGs have remained unnoticed in the exocrine pancreas, despite the fact that several studies have addressed the role of the actin terminal web in regulated exocytosis (9,(20)(21)(22).…”