Origin of Osteoclasts: Osteoclast Precursor Cells

Tsai, Jefferson; Kaneko, Kotomi; Suh, Andrew J.; Bockman, Richard S.; Park‐Min, Kyung‐Hyun

doi:10.11005/jbm.2023.30.2.127

Cited by 8 publications

(4 citation statements)

References 105 publications

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“…Contrarily, other studies have proven that OCLs are mainly derived from the classical CD14 + CD16 − monocyte population in healthy donors and patients with rheumatoid arthritis. It has also been described that CD14 + CD16 + monocytes can respond to RANKL to produce TNFα and IL-1 but cannot differentiate into osteoclasts [25]. Our results show that the predominant subset of circulating monocytes was the one defined as classical, which is in line with previous work [39,56].…”

Section: Discussionsupporting

confidence: 92%

“…The study of monocyte precursor populations of OCLs is complex, since there are various populations with distinctive characteristics and combinations of cell surface markers. The existence of three subpopulations of these cells is currently accepted, which show differences in their surface markers, phenotype, gene and protein expression, migration, cytokine secretion, and differentiation potential [25]. These subpopulations are known as classical (CD14 + /CD16 − ), intermediate (CD14 + /CD16 + ), and non-classical (CD14 −/+ CD16 ++ ) monocytes [26,27].…”

Section: Introductionmentioning

confidence: 99%

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New Insights into the Pro-Inflammatory and Osteoclastogenic Profile of Circulating Monocytes in Osteoarthritis Patients

Guillem-Llobat,

Marín,

Rouleau

et al. 2024

IJMS

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Osteoarthritis (OA) is a degenerative condition of the articular cartilage with chronic low-grade inflammation. Monocytes have a fundamental role in the progression of OA, given their implication in inflammatory responses and their capacity to differentiate into bone-resorbing osteoclasts (OCLs). This observational–experimental study attempted to better understand the molecular pathogenesis of OA through the examination of osteoclast progenitor (OCP) cells from both OA patients and healthy individuals (25 OA patients and healthy samples). The expression of osteoclastogenic and inflammatory genes was analyzed using RT-PCR. The OA monocytes expressed significantly higher levels of CD16, CD115, TLR2, Mincle, Dentin-1, and CCR2 mRNAs. Moreover, a flow cytometry analysis showed a significantly higher surface expression of the CD16 and CD115 receptors in OA vs. healthy monocytes, as well as a difference in the distribution of monocyte subsets. Additionally, the OA monocytes showed a greater osteoclast differentiation capacity and an enhanced response to an inflammatory stimulus. The results of this study demonstrate the existence of significant differences between the OCPs of OA patients and those of healthy subjects. These differences could contribute to a greater understanding of the molecular pathogenesis of OA and to the identification of new biomarkers and potential drug targets for OA.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

New Insights into the Pro-Inflammatory and Osteoclastogenic Profile of Circulating Monocytes in Osteoarthritis Patients

Guillem-Llobat,

Marín,

Rouleau

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

“…We found that the most predominant cells constituting the bone microenvironment were macrophages (56.4%). A large number of studies have demonstrated that macrophages can promote tumor progression and metastasis [33]. To further explore the role of macrophages in TNBC bone metastasis, we performed DEGs analysis on macrophages from CTRL and DHT-treated groups, and we found that macrophages in the DHT group showed a higher expression of genes associated with M2 polarization (e.g., Arg1 and Chil3), while genes associated with antigen presentation as well as M1-like phenotypes (e.g., IL1b, H2-Aa and H2-Eb1) were less expressed (Supplementary Fig.…”

Section: Activation Of Ar Allows Macrophages To Exhibit M2 Polarizati...mentioning

confidence: 99%

Androgen Receptor interacts with c-Myc to regulate macrophage-osteoclast axis and drive bone metastasis in Triple Negative Breast Cancer

Guan,

Liu,

Fan

et al. 2024

Preprint

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Breast cancer distant metastasis is known to exhibit organotropism, with triple negative breast cancer (TNBC) subtypes also displaying organ-specific metastasis. In publicly available clinical database of TNBC, we found that luminal androgen receptor-type (LAR) TNBC had a significant tendency for bone metastasis. In mouse models, we demonstrated that androgen receptor (AR) activation promoted LAR TNBC bone metastasis. Using single-cell sequencing, we discovered that c-Myc played a critical role in AR-mediated bone metastasis. Mechanistically, AR interacted with c-Myc, promoting the expression of c-Myc and consequently facilitating TNBC osteolytic bone metastasis. Further analysis of the bone microenvironment revealed that AR interactions with c-Myc not only mediated macrophage M2 polarization, but also promoted M2-type macrophage differentiation towards osteoclasts as well as osteoclast activation, ultimately promoting bone resorption effects. Collectively, these findings elucidate the mechanisms underlying bone metastasis in TNBC subtypes and inform potential interventions for TNBC bone metastasis.

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“…Specifically, in bone tissue, the GIPr is expressed in osteoblasts, osteocytes, and osteoclasts [ 16 , 17 , 18 ]. Osteoclasts, which are myeloid-derived multinucleated cells, resorb bone tissue and play a vital role in bone remodeling [ 19 ]. Excessive bone resorption caused by osteoclasts under pathological conditions leads to various diseases including rheumatoid arthritis and periodontitis [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

(D-Ala2)GIP Inhibits Inflammatory Bone Resorption by Suppressing TNF-α and RANKL Expression and Directly Impeding Osteoclast Formation

Lin,

Kitaura,

Ohori

et al. 2024

IJMS

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Glucose-insulinotropic polypeptide (GIP) is an incretin hormone that induces insulin secretion and decreases blood glucose levels. In addition, it has been reported to suppress osteoclast formation. Native GIP is rapidly degraded by dipeptidyl peptidase-4 (DPP-4). (D-Ala2)GIP is a newly developed GIP analog that demonstrates enhanced resistance to DPP-4. This study aimed to evaluate the influence of (D-Ala2)GIP on osteoclast formation and bone resorption during lipopolysaccharide (LPS)-induced inflammation in vivo and in vitro. In vivo, mice received supracalvarial injections of LPS with or without (D-Ala2)GIP for 5 days. Osteoclast formation and bone resorption were evaluated, and TNF-α and RANKL expression were measured. In vitro, the influence of (D-Ala2)GIP on RANKL- and TNF-α-induced osteoclastogenesis, LPS-triggered TNF-α expression in macrophages, and RANKL expression in osteoblasts were examined. Compared to the LPS-only group, calvariae co-administered LPS and (D-Ala2)GIP led to less osteoclast formation, lower bone resorption, and decreased TNF-α and RANKL expression. (D-Ala2)GIP inhibited osteoclastogenesis induced by RANKL and TNF-α and downregulated TNF-α expression in macrophages and RANKL expression in osteoblasts in vitro. Furthermore, (D-Ala2)GIP suppressed the MAPK signaling pathway. The results suggest that (D-Ala2)GIP dampened LPS-triggered osteoclast formation and bone resorption in vivo by reducing TNF-α and RANKL expression and directly inhibiting osteoclastogenesis.

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Origin of Osteoclasts: Osteoclast Precursor Cells

Cited by 8 publications

References 105 publications

New Insights into the Pro-Inflammatory and Osteoclastogenic Profile of Circulating Monocytes in Osteoarthritis Patients

New Insights into the Pro-Inflammatory and Osteoclastogenic Profile of Circulating Monocytes in Osteoarthritis Patients

Androgen Receptor interacts with c-Myc to regulate macrophage-osteoclast axis and drive bone metastasis in Triple Negative Breast Cancer

(D-Ala2)GIP Inhibits Inflammatory Bone Resorption by Suppressing TNF-α and RANKL Expression and Directly Impeding Osteoclast Formation

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