ArticleCalcified tissue international2023
Tumor Necrosis Factor-α Blunts the Osteogenic Effects of Muscle Cell-Derived Extracellular Vesicles by Affecting Muscle Cells.
Article in Calcified tissue international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Exosome-mediated muscle-bone crosstalk: mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- The Role of Extracellular Vesicles MicroRNAs in Sarcopenia: From Aging to Multi-Morbidity.Aging medicine (Milton (N.S.W)) · 2026Review
- Non-Bone-Derived Extracellular Vesicles in Osteoporosis: Evidence Mapping and Nanomedicine Translation.International journal of nanomedicine · 2026Review
- Bone-muscle interactions.Osteoporosis and sarcopenia · 2025Review
- RANKL-mediated osteoclastic subchondral bone loss at a very early stage precedes subsequent cartilage degeneration and uncoupled bone remodeling in a mouse knee osteoarthritis model.Journal of orthopaedic surgery and research · 2025Article
- CombiningFrontiers in cell and developmental biology · 2025Article
- Crosstalk between muscle and bone.Journal of bone and mineral metabolism · 2024Review
- The role and applications of extracellular vesicles in osteoporosis.Bone research · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular vesicles (EVs) play crucial roles in physiological and pathophysiological processes. Although studies have described muscle-bone interactions via humoral factors, we reported that EVs from C2C12 muscle cells (Myo-EVs) suppress osteoclast formation. Current clinical evidence suggests that inflammation induces both sarcopenia and osteoporosis. Although tumor necrosis factor-α (TNF-α) is a critical proinflammatory factor, the influences of TNF-α on muscle-bone interactions and Myo-EVs are still unclear. In the present study, we investigated the effects of TNF-α stimulation of C2C12 cells on osteoclast formation and osteoblastic differentiation modulated by Myo-EVs in mouse cells. TNF-α significantly decreased the protein amount in Myo-EVs, but did not affect the Myo-EV size distribution. TNF-α treatment of C2C12 myoblasts significantly decreased the suppression of osteoclast formation induced by Myo-EVs from C2C12 myoblasts in mouse bone marrow cells. Moreover, TNF-α treatment of C2C12 myoblasts in mouse preosteoclastic Raw 264.7 cells significantly limited the Myo-EV-induced suppression of osteoclast formation and decreased the Myo-EV-induced increase in mRNA levels of osteoclast formation-related genes. On the other hand, TNF-α treatment of C2C12 muscle cells significantly decreased the degree of Myo-EV-promoted mRNA levels of Osterix and osteocalcin, as well as ALP activity in mouse mesenchymal ST-2 cells. TNF-α also significantly decreased miR196-5p level in Myo-EVs from C2C12 myoblasts in quantitative real-time PCR. In conclusion, TNF-α stimulation of C2C12 muscle cells blunts both the osteoclast formation suppression and the osteoblastic differentiation promotion that occurs due to Myo-EVs in mouse cells. Thus, TNF-α may disrupt the muscle-bone interactions by direct Myo-EV modulation.
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Registered trials
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