PMID- 11726283
OWN - NLM
STAT- MEDLINE
DCOM- 20020419
LR  - 20190513
IS  - 0021-924X (Print)
IS  - 0021-924X (Linking)
VI  - 130
IP  - 6
DP  - 2001 Dec
TI  - Characterization of phagosomal subpopulations along endocytic routes in 
      osteoclasts and macrophages.
PG  - 823-31
AB  - Modifications occurring during the transformation of phagosomes into mature 
      phagolysosomes were investigated in osteoclast-like cells (OCLs) and macrophages 
      using latex beads as markers for the isolation of phagosomal compartments (LBC) 
      at different time points after phagocytosis. In OCLs, newly formed LBC acquired 
      cathepsin K, tartarate-resistant phosphatase (TRAP), lysosome-associated membrane 
      protein-1 (Lamp-1), and cathepsin D, and rapidly lost annexin II in a 
      time-dependent manner. The levels of Rab7 and c-Src in OCLs initially increased 
      and then gradually decreased during the transformation from early to late 
      endosomal LBC or phagolysosomes. Receptor activator of NF-kappaB (RANKL) 
      significantly increased the LBC levels of cathepsin K, TRAP, and c-Src, whereas 
      calcitonin decreased the LBC levels of cathepsin K, TRAP, and Rab7, indicating 
      that the transformation of early to late endosomal elements and lysosomes in OCLs 
      is also regulated by osteoclastogenesis regulatory factors. On the other hand, 
      changes in the LBC levels of Lamp-1, cathepsin D, and annexin II in macrophages 
      were comparable to those in OCLs. However, contrary to osteoclastic LBC, Rab7 
      levels of macrophage LBC decreased in a time-dependent manner. Macrophage LBC 
      were devoid of cathepsin K, TRAP, and c-Src in all transformation stages. These 
      observations suggest that OCLs and macrophages have different phagosome 
      maturation mechanisms that involve the specific and regulated acquisition of 
      markers from endocytic organelles. The results also demonstrate that the use of 
      LBC is a useful system in which to identify and characterize molecules involved 
      in these different endocytic pathways.
FAU - Sakai, E
AU  - Sakai E
AD  - Department of Pharmacology, Nagasaki University School of Dentistry, Nagasaki 
      852-8588, Japan.
FAU - Miyamoto, H
AU  - Miyamoto H
FAU - Okamoto, K
AU  - Okamoto K
FAU - Kato, Y
AU  - Kato Y
FAU - Yamamoto, K
AU  - Yamamoto K
FAU - Sakai, H
AU  - Sakai H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Biochem
JT  - Journal of biochemistry
JID - 0376600
RN  - 0 (Glycoproteins)
RN  - 0 (Osteoprotegerin)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tnfrsf11b protein, mouse)
RN  - 9007-12-9 (Calcitonin)
SB  - IM
MH  - Animals
MH  - Bone Marrow
MH  - Calcitonin/pharmacology
MH  - Endocytosis/*physiology
MH  - Glycoproteins/pharmacology
MH  - Kinetics
MH  - Macrophages/*physiology/ultrastructure
MH  - Male
MH  - Mice
MH  - Microscopy, Electron/methods
MH  - Microspheres
MH  - Osteoclasts/drug effects/*physiology/ultrastructure
MH  - Osteoprotegerin
MH  - Phagosomes/*classification/physiology/ultrastructure
MH  - Receptors, Cytoplasmic and Nuclear
MH  - Receptors, Tumor Necrosis Factor
EDAT- 2001/12/01 10:00
MHDA- 2002/04/20 10:01
CRDT- 2001/12/01 10:00
PHST- 2001/12/01 10:00 [pubmed]
PHST- 2002/04/20 10:01 [medline]
PHST- 2001/12/01 10:00 [entrez]
AID - 10.1093/oxfordjournals.jbchem.a003054 [doi]
PST - ppublish
SO  - J Biochem. 2001 Dec;130(6):823-31. doi: 10.1093/oxfordjournals.jbchem.a003054.