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Titolo:
Isoproterenol inhibits fluid-phase endocytosis from early to late endosomes
Autore:
Sojakka, K; Punnonen, EL; Marjomaki, VS;
Indirizzi:
Univ Jyvaskyla, Dept Biol & Environm Sci, FIN-40351 Jyvaskyla, Finland Univ Jyvaskyla Jyvaskyla Finland FIN-40351 FIN-40351 Jyvaskyla, Finland
Titolo Testata:
EUROPEAN JOURNAL OF CELL BIOLOGY
fascicolo: 3, volume: 78, anno: 1999,
pagine: 161 - 169
SICI:
0171-9335(199903)78:3<161:IIFEFE>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
MANNOSE 6-PHOSPHATE RECEPTOR; CARDIAC MYOCYTES; CYTOPLASMIC PH; TRANSPORT; CELLS; REDISTRIBUTION; TRAFFICKING; LYSOSOMES; VESICLES; PATHWAY;
Keywords:
endocytosis; isoproterenol; membrane transport;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Marjomaki, VS Univandvaskyla, Dept Biol & Environm Sci, POB 35, FIN-40351 Jyvaskyla, Finl Univ Jyvaskyla POB 35 Jyvaskyla Finland FIN-40351 yla, Finl
Citazione:
K. Sojakka et al., "Isoproterenol inhibits fluid-phase endocytosis from early to late endosomes", EUR J CELL, 78(3), 1999, pp. 161-169

Abstract

We have shown recently that isoproterenol affects both the cellular location and the morphology of late endosomes in a pa-dependent manner [Marjomakiet al,, Eur. J. Cell Biol, 65, 1-13 (1994)]. In this study, using fluorescence and quantitative electron microscopy, we wanted to examine further what is the fate of internalized markers during their translocation from earlyto late endosomes under isoproterenol treatment. Fluorescein dextran internalized for 30 min (10-min pulse followed by a 20-min chase) showed accumulation in the cellular periphery during isoproterenol treatment in contrast to the control cells, which accumulated dextran in the perinuclear region. Quantitative electron microscopy showed that the markers accumulated in theearly endosomes and putative carrier vesicles, In addition, different particulate markers that were internalized sequentially accumulated in similar structures due to the isoproterenol treatment, altogether suggesting that isoproterenol retards the translocation of markers to the later structures. Prelabelling of the late endosomes with fluorescent dextran or BSA-coated gold particles showed that isoproterenol causes a reduction of the mean sizeof the prelabelled late endosomes as well as a shift of these vesicles to the cellular periphery. Isoproterenol had no apparent effect on the morphology nor on the location of lysosomes, Percoll fractionation shelved that the changes in late endosomal location and morphology did not change their characteristic density. Furthermore, electron microscopy showed that, in the cellular periphery, these late endosomal elements did not fuse with early endosomal structures, which is in agreement with the results of biochemical in vitro cell-free assays carried out by others. In conclusion, the resultsshow that isoproterenol inhibits transport from early to late endosomes ina manner that may be pH- and/or Ca2+-dependent. Simultaneously, isoproterenol causes fragmentation of the late endosomal compartment and the shift ofthese fragments to the cellular periphery, where they have a restricted ability to fuse with earlier endosomal structures.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 12:01:10