ArticleFrontiers in pharmacology2026
PDGF-BB inhibits SP1/Angptl7 mediated chondro-endothelial crosstalk via stress-sensitivity Piezo1 regulation in osteoarthritis.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Osteoarthritis (OA) involves cartilage degradation and subchondral bone alterations, yet the mechanisms of chondro-endothelial crosstalk remain unclear. Stress-sensitive Piezo1 and SP1/Angptl7 signaling may play key roles in this process. This research aimed to investigate whether Platelet-derived growth factor (PDGF)-BB regulates chondro-endothelial crosstalk via Piezo1-mediated SP1/Angptl7 inhibition. Methods: Single- and multiple-cell-component organoids (chondrocytes SW1353 and endothelial HMEC-1) were constructed using high-throughput 3D culture. Organoids were treated with MIA to induce OA-like changes, followed by PDGF-BB with or without Yoda1 (Piezo1 activator) or Angptl7. Results: PDGF-BB inhibited F-actin formation and reduced Piezo1 activation in OA chondrocytes. It suppressed SP1 phosphorylation and Angptl7 expression, downregulating VEGF/Notch/DLL4 signaling and reducing endothelial invasion in organoids. These effects were partially reversed by Yoda1 and fully reversed by Angptl7. Discussion: PDGF-BB alleviates OA by inhibiting SP1/Angptl7-mediated chondro-endothelial crosstalk, partially via stress-sensitive Piezo1 regulation through cytoskeletal remodeling. Multiple-cell-component organoids provide a valuable
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