Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-10-13
pubmed:abstractText
Upon activation of human neutrophils by chemoattractants, functionally important proteins are rapidly transported from intracellular granules and storage vesicles to the plasma membrane. This is accompanied by a marked increase in the rate of endocytosis and by ligand-independent internalization of type 1 complement receptors (CR1). To define the pathway of endocytosis, we used gold-conjugated BSA in a pulse-chase protocol. This tracer was initially internalized into small endocytic vesicles which rapidly traversed the cytoplasm and coalesced to form large, conspicuous multivesicular bodies. Within 5 min after addition of the chemoattractant, multivesicular bodies contained > 60% of the cell-associated BSA-gold. CR1 colocalized with the endocytic tracer in both the early endosomes and multivesicular bodies. In unstimulated cells, there was much less uptake of BSA-gold and multivesicular bodies were rarely seen. Using the acidotropic amine, DAMP, and anti-DNP antibodies, we found that the multivesicular bodies were acidified but the early endosomes did not concentrate DAMP. Neither the early endosomes nor the multivesicular bodies initially contained the lysosomal membrane antigens hLAMP 1 or 2, but hLAMP-positive structures subsequently joined the multivesicular bodies. The rapid activation of the endocytic pathway upon stimulation of neutrophils allowed us to visualize the de novo formation and maturation of multivesicular bodies. Our observations suggest that vesicles containing ion pumps and acid hydrolases fuse with multivesicular bodies, giving them characteristics of lysosomes, and that these are the probable sites of degradation of CR1. The observations do not support models which would require transport of CR1 from multivesicular bodies to defined, pre-existing lysosomes for degradation.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1378856, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1386610, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1407546, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-14731803, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1560027, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1679012, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1729356, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1826092, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-1826558, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2136801, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2161041, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2298916, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2344614, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2374607, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2423307, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2446314, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2824654, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2849607, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2868013, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2912382, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2933416, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2965151, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-2990909, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-3020987, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-3080437, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-3856853, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-3882239, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-3972894, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-4118890, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-4180353, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-4729503, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6146980, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6173220, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6209300, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6218336, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6237120, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6288298, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6304114, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6821528, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6847888, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-6924936, http://linkedlifedata.com/resource/pubmed/commentcorrection/8083352-7440248
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1113-25
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Internalization of type 1 complement receptors and de novo multivesicular body formation during chemoattractant-induced endocytosis in human neutrophils.
pubmed:affiliation
Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, U.S. Gov't, P.H.S.