ArticleThe Journal of biological chemistry2010
Serum calcium-decreasing factor, caldecrin, inhibits osteoclast differentiation by suppression of NFATc1 activity.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Geranylgeraniol promotes osteoblast differentiation and inhibits osteoclastogenesis through MAPK and nuclear receptor signaling.The Journal of biological chemistry · 2026Article
- Boric Acid Inhibits RANKL-Stimulated Osteoclastogenesis In Vitro and Attenuates LPS-Induced Bone Loss In Vivo.Biological trace element research · 2023Article
- Reduction of Osteoclastic Differentiation of Raw 264.7 Cells by EMF Exposure through TRPV4 and p-CREB Pathway.International journal of molecular sciences · 2023Article
- Lonafarnib Inhibits Farnesyltransferase via Suppressing ERK Signaling Pathway to Prevent Osteoclastogenesis in Titanium Particle-Induced Osteolysis.Frontiers in pharmacology · 2022Article
- TRPV6 is a potential regulator of bone resorption in bone loss induced by estrogen deficiency.iScience · 2021Article
- Purification and Biological Function of Caldecrin.Medicines (Basel, Switzerland) · 2021Review
- Biological Effects of β-Glucans on Osteoclastogenesis.Molecules (Basel, Switzerland) · 2021Review
- The calcium channel TRPV6 is a novel regulator of RANKL-induced osteoclastic differentiation and bone absorption activity through the IGF-PI3K-AKT pathway.Cell proliferation · 2021Article
- Overview of RAW264.7 for osteoclastogensis study: Phenotype and stimuli.Journal of cellular and molecular medicine · 2019Review
- Screening for natural medicines effective for the treatment of osteoporosis.Journal of natural medicines · 2019Article
- Rosiglitazone suppresses RANKL-induced NFATc1 autoamplification by disrupting the physical interaction between NFATc1 and PPARγ.FEBS open bio · 2018Article
- Caldecrin: A pancreas-derived hypocalcemic factor, regulates osteoclast formation and function.World journal of biological chemistry · 2015Review
- Rhinacanthin C Inhibits Osteoclast Differentiation and Bone Resorption: Roles of TRAF6/TAK1/MAPKs/NF-κB/NFATc1 Signaling.PloS one · 2015Article
- The role of calcium and nicotinic acid adenine dinucleotide phosphate (NAADP) in human osteoclast formation and resorption.Calcified tissue international · 2015Article
- Zinc inhibits osteoclast differentiation by suppression of Ca2+-Calcineurin-NFATc1 signaling pathway.Cell communication and signaling : CCS · 2013Article
- Serum calcium-decreasing factor, caldecrin, inhibits receptor activator of NF-κB ligand (RANKL)-mediated Ca2+ signaling and actin ring formation in mature osteoclasts via suppression of Src signaling pathway.The Journal of biological chemistry · 2012Article
- Chymotrypsin C (caldecrin) is associated with enamel development.Journal of dental research · 2011Article
- Chymotrypsin C mutations in chronic pancreatitis.Journal of gastroenterology and hepatology · 2011Review
- Nucleosides accelerate inflammatory osteolysis, acting as distinct innate immune activators.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2011Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caldecrin/chymotrypsin C is a novel secretory-type serine protease that was originally isolated as a serum calcium-decreasing factor from the pancreas. Previously, we reported that caldecrin suppressed the bone-resorbing activity of rabbit mature osteoclasts (Tomomura, A., Yamada, H., Fujimoto, K., Inaba, A., and Katoh, S. (2001) FEBS Lett. 508, 454-458). Here, we investigated the effects of caldecrin on mouse osteoclast differentiation induced by macrophage-colony stimulating factor and the receptor activator of NF-kappaB ligand (RANKL) from the monocyte/macrophage cell lineage of bone marrow cells. Wild-type and protease-deficient mutant caldecrin dose-dependently inhibited RANKL-stimulated tartrate-resistant acid phosphatase-positive osteoclast formation from bone marrow cells. Caldecrin did not affect macrophage colony formation from monocyte/macrophage lineage cells or osteoclast progenitor generation in cultures of bone marrow cells. Caldecrin inhibited accumulation of the RANKL-stimulated nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) mRNA in bone marrow cells, which is a key transcription factor for the differentiation of osteoclasts. Caldecrin also suppressed RANKL-induced differentiation of the RAW264.7 monocyte/macrophage cell line into osteoclasts. Caldecrin reduced the transcriptional activity of NFATc1 in RAW264.7 cells, whereas those of NF-kappaB and c-Fos, which are also transcription factors involved in osteoclast differentiation, were unaffected. Caldecrin inhibited RANKL-stimulated nuclear translocation of NFATc1 and the activity of the calcium/calmodulin-dependent phosphatase, calcineurin. Caldecrin inhibited phospholipase Cgamma1-mediated Ca(2+) oscillation evoked by RANKL stimulation. RANKL-stimulated phosphorylation of spleen tyrosine kinase (Syk) was also attenuated by caldecrin. Taken together, these results indicate that caldecrin inhibits osteoclastogenesis, without its protease activity, by preventing a phospholipase Cgamma1-mediated Ca(2+)oscillation-calcineurin-NFATc1 pathway.
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