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The enigmatic function of TREM-2 in osteoclastogenesis
Colonna M, Turnbull I, Klesney-Tait J.. Advances in experimental medicine and biology, 2007-01-01
Topic: Brain proteins, microglia and lab models
The triggering receptor expressed on myeloid cells 2 (TREM-2) is a member of family of receptors that play a central role in regulating function of myeloid cells. TREM-2 is expressed on macrophages, microglia and pre-osteoclasts and transduces intracellular signals through the adaptor DAP12. In human, genetic defects of TREM-2 and DAP12 result in a rare syndrome characterized by presenile dementia and bone cysts. This syndrome and the tissue distribution of TREM-2 have indicated a role of the TREM-2/DAP12 complex in brain function and bone modeling, particularly osteoclastogenesis. Accordingly, human TREM-2- and DAP12-deficient pre-osteoclast precursors failed to differentiate in vitro into mature osteoclasts endowed with bone resorptive activity. In mouse, DAP12-deficiency also resulted in impaired osteoclastogenesis in vitro and a mild osteopetrosis in vivo although bone cysts were not observed. Surprisingly, TREM-2-deficiency in mouse led to accelerated osteoclastogenesis in vitro without osteopetrosis or bone cysts in vivo, revealing an unexpected inhibitory function of mouse TREM-2. These data demonstrate that TREM-2 function is essential for normal osteoclastogenesis. The conflicting results as to the relationship between TREM-2, DAP12 and osteoclastogenesis and bone modeling in human and mouse suggest that TREM-2 contribution to osteoclast biology may vary depending on the influence of additional DAP12-associated receptors and on the presence of TREM-2 ligands with variable avidity/affinity, which may induce either activating or an inhibitory signals through TREM-2/DAP12.
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APA 7th
Colonna, M., Turnbull, I., & Klesney-Tait, J. (2007). The enigmatic function of TREM-2 in osteoclastogenesis. Advances in experimental medicine and biology. https://doi.org/10.1007/978-0-387-72009-8_13
Vancouver
Colonna M, Turnbull I, Klesney-Tait J. The enigmatic function of TREM-2 in osteoclastogenesis. Advances in experimental medicine and biology. 2007. doi:10.1007/978-0-387-72009-8_13. PMID: 17966394.
BibTeX
@article{colonna2007-17966394,
author = {Colonna, M. and Turnbull, I. and Klesney-Tait, J.},
title = {{The enigmatic function of TREM-2 in osteoclastogenesis}},
journal = {Advances in experimental medicine and biology},
year = {2007},
doi = {10.1007/978-0-387-72009-8_13},
pmid = {17966394},
url = {https://doi.org/10.1007/978-0-387-72009-8_13}
}
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Key findings
- In human, genetic defects of TREM-2 and DAP12 result in a rare syndrome characterized by presenile dementia and bone cysts.
- The conflicting results as to the relationship between TREM-2, DAP12 and osteoclastogenesis and bone modeling in human and mouse suggest that TREM-2 contribution to osteoclast biology may vary depending on the influence of additional DAP12-associated receptors and on the presence of TREM-2 ligands with variable avidity/affinity, which may induce either activating or an inhibitory signals through TREM-2/DAP12.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Advances in experimental medicine and biology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2007 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17966394) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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