Ca++-dependent disassembly and reassembly of occluding junctions in guinea pig pancreatic acinar cells. Effect of drugs.

摘要: Incubation of guinea pig pancreatic lobules in Ca++-free Krebs-Ringer bicarbonate solution (KRB) containing 0.5 mM ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N'-tetraacetate (EGTA) results the progressive fragmentation occluding zonulae (ZO) with formation multiple discrete junctions (fasciae occludentes) localized lateral and lumenal plasmalemma. After 1--2 h such incubation, most ZO appear completely disassembled. This disappearance heterogeneity density intramembrane particles on P-fracture faces basolateral If Ca++ ions are reintroduced into incubation fluid at this point, continous reform around apices cells; contrast, (imp) plasmalemma remains same as region, least for 3 after reintroduction. When added to fluid, cycloheximide (at a dose known inhibit protein synthesis greater than 95%) cytochalasin B doses which disrupt microfilaments modify cell shape) had no effect organization ZO, their disassembly Ca++-free, EGTA medium, or Ca++-dependent reformation. Likewise, were unaffected by colchicine; however, treatment latter drug reassembly was defective, strand networks surface incomplete segregation region. Antimycin A, other hand, when Ca++-EGTA induced large proliferation long, infrequently anastomosed junctional strands, usually arranged form ribbons, festoons, bizarre arrays. The possible relationship these vitro findings vivo biogenesis turnover is discussed. It suggested that impairment colchicine might be correlated disorder general exocrine cells. Moreover, antimycin A could act promoting aggregation pool free components (or precursors) exist normally