Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P17931 (
galectin-3
)
2,860
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Galectin-3
is a beta-galactoside-binding animal lectin having pleiotropic effects on cell growth, differentiation, and apoptosis. This lectin has been shown to be involved in phagocytosis by macrophages and in inflammation. Here we investigated an involvement of
galectin-3
in the regulatory process of inflammatory bone resorption in rats with adjuvant-induced arthritis (AA rats) accompanying severe bone destruction in the ankle joints. The protein level of
galectin-3
in the ankle-joint extracts was markedly augmented at week 3 after adjuvant injection, at the time when severe bone destruction was observed. Immunohistochemical analysis revealed an extremely high expression of
galectin-3
in macrophages and granulocytes infiltrated in the area of severe bone destruction. To estimate the role of
galectin-3
in osteoclastogenesis and osteoclastic bone resorption, recombinant
galectin-3
was added to in vitro culture systems.
Galectin-3
markedly inhibited the formation of osteoclasts in cultures of murine osteoclast precursor cell line as well as in rat bone marrow culture systems. This inhibition was not observed by heat-inactivated
galectin-3
or by galectin-7. Although recombinant
galectin-3
did not affect signaling through mitogen-activated protein kinase (MAPK) or nuclear factor-kappaB (NF-kappaB), it specifically suppressed the induction of
nuclear factor of activated T-cells
c1 (NFATc1).
Galectin-3
significantly inhibited dentine resorption by mature osteoclasts in vitro. Furthermore, in vivo studies clearly showed a significant suppression of bone destruction and osteoclast recruitment accompanying arthritis, when
galectin-3
was injected into the cavity of ankle joint of AA rats. Thus, abundant
galectin-3
observed in the area of severe bone destruction may act as a negative regulator for the upregulated osteoclastogenesis accompanying inflammation to prevent excess bone destruction.
...
PMID:A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats. 1901 43