File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1007/s00011-022-01608-9
- Scopus: eid_2-s2.0-85135228821
- PMID: 35916930
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Human mast cells induce osteoclastogenesis through cell surface RANKL
Title | Human mast cells induce osteoclastogenesis through cell surface RANKL |
---|---|
Authors | |
Keywords | Mast cell Osteoclast Osteoclastogenesis Osteoporosis RANKL |
Issue Date | 2022 |
Citation | Inflammation Research, 2022, v. 71, n. 10-11, p. 1261-1270 How to Cite? |
Abstract | Objectives: We employed the co-culture of CD34+ stem cell-derived human mast cells (HMC) and human monocyte-derived osteoclast precursors to evaluate if mast cells contribute to the pathogenesis of osteoporosis through regulation of osteoclast proliferation and activation. Methods: Mature HMC and osteoclast precursors were cultured from monocytes isolated from human buffy coat. The osteoclast precursors were incubated with HMC or receptor activator of nuclear factor kappa-B ligand (RANKL) for a week prior to determination of osteoclast maturation through characterization by their morphology and tartrate resistant acid phosphatase (TRAP) expression. The bone absorption activity was determined by pit formation on osteo-assay plate. Results: Mature osteoclasts were identified following co-culture of osteoclast precursors with HMC for one week in the absence of RANKL and they were capable of bone resorption. These actions of HMC on osteoclasts were not affected by mast cell activators such anti-IgE or substance P but could be reversed by osteoprotegerin (OPG) in the co-culture system suggesting the involvement of RANKL. The expression of RANKL on the cell surface of HMC was confirmed by flow cytometry and the density was not affected by activation of HMC. Conclusion: Our study provided direct evidence confirming the initiation of osteoclast proliferation and activation by mast cells through cell surface RANKL suggesting that mast cells may contribute to bone destruction in pathological conditions such as osteoporosis. |
Persistent Identifier | http://hdl.handle.net/10722/343387 |
ISSN | 2023 Impact Factor: 4.8 2023 SCImago Journal Rankings: 1.309 |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ng, Chun Wai | - |
dc.contributor.author | Chan, Ben Chung Lap | - |
dc.contributor.author | Ko, Chun Hay | - |
dc.contributor.author | Tam, Issan Yee San | - |
dc.contributor.author | Sam, Sze Wing | - |
dc.contributor.author | Lau, Clara Bik San | - |
dc.contributor.author | Leung, Ping Chung | - |
dc.contributor.author | Lau, Hang Yung Alaster | - |
dc.date.accessioned | 2024-05-10T09:07:41Z | - |
dc.date.available | 2024-05-10T09:07:41Z | - |
dc.date.issued | 2022 | - |
dc.identifier.citation | Inflammation Research, 2022, v. 71, n. 10-11, p. 1261-1270 | - |
dc.identifier.issn | 1023-3830 | - |
dc.identifier.uri | http://hdl.handle.net/10722/343387 | - |
dc.description.abstract | Objectives: We employed the co-culture of CD34+ stem cell-derived human mast cells (HMC) and human monocyte-derived osteoclast precursors to evaluate if mast cells contribute to the pathogenesis of osteoporosis through regulation of osteoclast proliferation and activation. Methods: Mature HMC and osteoclast precursors were cultured from monocytes isolated from human buffy coat. The osteoclast precursors were incubated with HMC or receptor activator of nuclear factor kappa-B ligand (RANKL) for a week prior to determination of osteoclast maturation through characterization by their morphology and tartrate resistant acid phosphatase (TRAP) expression. The bone absorption activity was determined by pit formation on osteo-assay plate. Results: Mature osteoclasts were identified following co-culture of osteoclast precursors with HMC for one week in the absence of RANKL and they were capable of bone resorption. These actions of HMC on osteoclasts were not affected by mast cell activators such anti-IgE or substance P but could be reversed by osteoprotegerin (OPG) in the co-culture system suggesting the involvement of RANKL. The expression of RANKL on the cell surface of HMC was confirmed by flow cytometry and the density was not affected by activation of HMC. Conclusion: Our study provided direct evidence confirming the initiation of osteoclast proliferation and activation by mast cells through cell surface RANKL suggesting that mast cells may contribute to bone destruction in pathological conditions such as osteoporosis. | - |
dc.language | eng | - |
dc.relation.ispartof | Inflammation Research | - |
dc.subject | Mast cell | - |
dc.subject | Osteoclast | - |
dc.subject | Osteoclastogenesis | - |
dc.subject | Osteoporosis | - |
dc.subject | RANKL | - |
dc.title | Human mast cells induce osteoclastogenesis through cell surface RANKL | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1007/s00011-022-01608-9 | - |
dc.identifier.pmid | 35916930 | - |
dc.identifier.scopus | eid_2-s2.0-85135228821 | - |
dc.identifier.volume | 71 | - |
dc.identifier.issue | 10-11 | - |
dc.identifier.spage | 1261 | - |
dc.identifier.epage | 1270 | - |
dc.identifier.eissn | 1420-908X | - |