Macrophage galactose lectin is critical for Kupffer cells to clear aged platelets.
Animals
Antibodies
/ immunology
Asialoglycoproteins
/ immunology
Blood Platelets
/ metabolism
Cells, Cultured
Galactose
/ metabolism
Healthy Volunteers
Humans
Kupffer Cells
/ metabolism
Lectins, C-Type
/ immunology
Membrane Proteins
/ immunology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Phagocytosis
Staphylococcal Infections
/ metabolism
Staphylococcus aureus
/ metabolism
Journal
The Journal of experimental medicine
ISSN: 1540-9538
Titre abrégé: J Exp Med
Pays: United States
ID NLM: 2985109R
Informations de publication
Date de publication:
06 04 2020
06 04 2020
Historique:
received:
22
04
2019
revised:
01
10
2019
accepted:
17
12
2019
entrez:
25
1
2020
pubmed:
25
1
2020
medline:
11
11
2020
Statut:
ppublish
Résumé
Every day, megakaryocytes produce billions of platelets that circulate for several days and eventually are cleared by the liver. The exact removal mechanism, however, remains unclear. Loss of sialic acid residues is thought to feature in the aging and clearance of platelets. Using state-of-the-art spinning disk intravital microscopy to delineate the different compartments and cells of the mouse liver, we observed rapid accumulation of desialylated platelets predominantly on Kupffer cells, with only a few on endothelial cells and none on hepatocytes. Kupffer cell depletion prevented the removal of aged platelets from circulation. Ashwell-Morell receptor (AMR) deficiency alone had little effect on platelet uptake. Macrophage galactose lectin (MGL) together with AMR mediated clearance of desialylated or cold-stored platelets by Kupffer cells. Effective clearance is critical, as mice with an aged platelet population displayed a bleeding phenotype. Our data provide evidence that the MGL of Kupffer cells plays a significant role in the removal of desialylated platelets through a collaboration with the AMR, thereby maintaining a healthy and functional platelet compartment.
Identifiants
pubmed: 31978220
pii: 133651
doi: 10.1084/jem.20190723
pmc: PMC7144524
pii:
doi:
Substances chimiques
Antibodies
0
Asialoglycoproteins
0
CLEC10A protein, human
0
Clec10a protein, mouse
0
Lectins, C-Type
0
MGL2 protein, mouse
0
Membrane Proteins
0
Galactose
X2RN3Q8DNE
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NHLBI NIH HHS
ID : P01 HL131474
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK048247
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL125352
Pays : United States
Organisme : CIHR
Pays : Canada
Informations de copyright
© 2020 Crown copyright. The government of Australia, Canada, or the UK ("the Crown") owns the copyright interests of authors who are government employees. The Crown Copyright is not transferable.
Déclaration de conflit d'intérêts
Disclosures: The authors declare no competing interests exist.
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