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Effect of cholera toxin and cyclic adenosine monophosphate on fluid‐phase endocytosis, distribution, and trafficking of endosomes in rat liver
Author(s) -
Van Dyke Rebecca W.
Publication year - 2000
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2000.19790
Subject(s) - endosome , endocytosis , microbiology and biotechnology , cholera toxin , cyclic adenosine monophosphate , biology , hepatocyte , vesicle , golgi apparatus , biochemistry , receptor , intracellular , endocrinology , membrane , endoplasmic reticulum , in vitro
In prior studies, we showed that cholera (CTX) and pertussis toxins (PTX) increase rat liver endosome acidification. This study was performed to characterize the effects of these toxins and cyclic adenosine monophosphate (cAMP) on endosome ion transport, fluid‐phase endocytosis (FPE), and endosome trafficking in liver. In control liver, more mature populations of endosomes acidified progressively more slowly, but both toxins and cAMP caused retention of an early endosome acidification profile in maturing endosomes. CTX caused a density shift in endosomes, and all agents increased net FPE at time points from 5 to 60 minutes. By confocal microscopy, fluorescent dextrans first appeared in small vesicles at the hepatocyte sinusoidal membrane and trafficked rapidly to the pericanalicular area, near lysosomes and the trans‐Golgi network (TGN). Prolonged exposure to these agents caused redistribution of many labeled vesicles to the perinuclear region, colocalized with markers of both early (EEA1 and transferrin receptor) and late (LAMP1) endosomes. We conclude that cAMP is the common agent that disrupted normal maturation and trafficking of endosomes and increased net FPE, in part via decreased diacytosis.