ArticleJournal of dental research2014
CCL7 is a protective factor secreted by mechanically loaded osteocytes.
Article in Journal of dental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Insights into the mechanism of vascular endothelial cells on bone biology.Bioscience reports · 2021Pooled it
- Osteocyte Cell-Cell Communication Within and Beyond Bone.Current osteoporosis reports · 2026Review
- The MCP-3/Ccr3 axis contributes to increased bone mass by affecting osteoblast and osteoclast differentiation.Experimental & molecular medicine · 2024Article
- Efficient improvement of the proliferation, differentiation, and anti-arthritic capacity of mesenchymal stem cells by simply culturing on the immobilized FGF2 derived peptide, 44-ERGVVSIKGV-53.Journal of advanced research · 2024Article
- Genetic diversity modulates the physical and transcriptomic response of skeletal muscle to simulated microgravity in male mice.NPJ microgravity · 2023Article
- Fluid flow shear stress and tissue remodeling-an orthodontic perspective: evidence synthesis and differential gene expression network analysis.Frontiers in bioengineering and biotechnology · 2023Article
- CCL7 playing a dominant role in recruiting early OCPs to facilitate osteolysis at metastatic site of colorectal cancer.Cell communication and signaling : CCS · 2022Article
- Osteocyte apoptosis: the roles and key molecular mechanisms in resorption-related bone diseases.Cell death & disease · 2020Review
- The neuropeptide calcitonin gene-related peptide alpha is essential for bone healing.EBioMedicine · 2020Article
- Old Mice Have Less Transcriptional Activation But Similar Periosteal Cell Proliferation Compared to Young-Adult Mice in Response to in vivo Mechanical Loading.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Mechanical Loading Attenuates Radiation-Induced Bone Loss in Bone Marrow Transplanted Mice.PloS one · 2016Article
- IL-6 and IGF-1 Signaling Within and Between Muscle and Bone: How Important is the mTOR Pathway for Bone Metabolism?Current osteoporosis reports · 2015Review
- Differential Influence ofIn vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
In a search for factors up-regulated by mechanical strain in osteocytes, we discovered that chemokine (C-C motif) ligand 7 (CCL7), a chemotactic myokine, was highly expressed in MLO-Y4 osteocyte-like cells. Although MLO-Y4 cells secrete potent chemotactic factors for osteoclast precursors, CCL7 was not responsible for this activity. CCL7 was increased in osteocytes in response to tooth movement in vivo. Since mechanical loading plays a crucial role in maintaining osteocyte viability, CCL7 was tested for protective activity and found to be protective against cell death induced by dexamethasone and etoposide. CCL7 specific antibody partially, but in combination with indomethacin, completely abrogated the protective effects of fluid flow shear stress against dexamethasone-induced cell death. CCL7 activated the β-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this pathway is responsible for the observed protective effects. A related cytokine, CCL2, also produced by MLO-Y4 cells but not regulated by mechanical loading, proved to be more potent and protected against cell death induced by not only dexamethasone, but also by Tumor Necrosis Factor α (TNFα). Whereas osteocytes may produce CCL2 in constitutively low levels, a major function of mechanically induced CCL7 may be to selectively protect osteocytes in an autocrine manner against glucocorticoid-induced cell death.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.