ArticleFrontiers in cell and developmental biology2023
The actin-bundling protein, PLS3, is part of the mechanoresponsive machinery that regulates osteoblast mineralization.
Article in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 3 citations in OpenAlex.
- Multiscale analysis and functional validation of the cellular and genetic determinants of skeletal disease.Nature genetics · 2026Article
- Multiscale analysis and functional validation of the cellular and genetic determinants of skeletal disease.bioRxiv : the preprint server for biology · 2026Article
- The Role of Plastin in Bone, Cartilage, and Related Diseases.Calcified tissue international · 2026Review
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Article
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4 authors at 1 institution in 1 country.
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Abstract
Plastin-3 (PLS3) is a calcium-sensitive actin-bundling protein that has recently been linked to the development of childhood-onset osteoporosis. Clinical data suggest that PLS3 mutations lead to a defect in osteoblast function, however the underlying mechanism remains elusive. To investigate the role of PLS3 in bone mineralization, we generated MC3T3-E1 preosteoblast cells that are stably depleted of PLS3. Analysis of osteogenic differentiation of control and PLS3 knockdown (PLS3 KD) cells showed that depletion of PLS3 does not alter the first stage of osteoblast mineralization in which a collagen matrix is deposited, but severely affects the subsequent mineralization of that matrix. During this phase, osteoblasts heavily rely on mechanosensitive signaling pathways to sustain mineral deposition in response to increasing stiffness of the extracellular matrix (ECM). PLS3 prominently localizes to focal adhesions (FAs), which are intricately linked to mechanosensation. In line with this, we observed that depletion of PLS3 rendered osteoblasts unresponsive to changes in ECM stiffness and showed the same cell size, FA lengths and number of FAs when plated on soft (6 kPa)
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