ArticleCells2026
MACF1 Mediates the Impairment of Mechanical Unloading on Osteoblast Differentiation via F-Actin/ERK/Runx2 Axis.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Mechanical Unloading Inhibits Osteoblast Differentiation via Downregulation of OGT-Mediated O-GlcNAcylation.Current issues in molecular biology · 2026Article
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8 authors.
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Abstract
Decreased osteoblast differentiation contributes to bone loss induced by mechanical unloading. However, the underlying mechanism is still unclear. We previously found that microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal protein, plays an important role in regulating osteoblast differentiation, while the role of MACF1 in mechanical unloading suppressing osteoblast differentiation remains unclear. Here, an MACF1-knockdown (MACF1-KD) osteoblast cell line and primary osteoblasts were subjected to mechanical unloading conducted by a random positioning machine (RPM). Osteoblast differentiation was evaluated by alkaline phosphatase (ALP) staining and real-time PCR. F-actin distribution was examined by immunofluorescence staining. Western blot was adopted to detect the protein levels. Moreover, cytochalasin B and PD98059 were applied to disrupt F-actin and inhibit extracellular signal-regulated kinase (ERK) activity, respectively, to confirm the mechanism. The results show that MACF1 is significantly downregulated in osteoblasts by mechanical unloading together with decreased osteoblast differentiation. MACF1-KD osteoblasts exhibit reduced differentiation capacity and are insensitive to mechanical unloading. Mechanistically, MACF1 mediates the suppression of mechanical unloading on osteoblast differentiation by regulating F-actin distribution and the downstream ERK/Runx2 signaling. Furthermore, F-actin disruption and ERK inhibition assays confirm that MACF1 mediates the impairment of mechanical unloading on osteoblast differentiation via the F-actin/ERK/Runx2 axis. In conclusion, this study reveals MACF1 as a mechanotransduction mediator for mechanical unloading, inhibiting osteoblast differentiation via F-actin/ERK/Runx2, and contributes to a novel mechanistic insight of cell mechanotransduction.
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