Plastin-3 contributes to articular cartilage degeneration

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Introduction Plastin-3 (PLS3) is a ubiquitously expressed actin-binding and -bundling protein which influences F-actin dynamics affecting various cellular processes [ 1 ]. Recently it has been found that PLS3 levels in chondrocytes correlate with the degree of cartilage degeneration in human osteoarthritis (OA) [ 2 ]. The aim of our study was to characterize the impact of both, Pls3 deficiency (KO) and PLS3 overexpression (OE) on articular cartilage in mice. Material and Methods We analyzed ubiquitous 6-month-old female Pls3 KO [ 3 ] and PLS3 OE (homozygous PLS3V5 transgene) mice [ 4 ] in comparison to the C57BL/6N (WT) mice (n=3–8). Mechanical properties of articular cartilage were measured by AFM. Structural degeneration was determined using a modified Osteoarthritis Research Society International (OARSI) score [ 5 ]. Immunohistochemical stainings of collagen-type-II and MMP13 were performed. Bone structural parameters were analyzed using µCT. Chondrocytes from newborn mice were isolated to study F-actin structures via immunofluorescence. Results OARSI score was significantly enhanced (p<0.05) (OE:2.63±1.52; WT:0.42±0.58). Accordingly, the elastic modulus was significantly (p<0.05) decreased (OE:0.305±0.189 MPa; WT:0.909±0.634 MPa). A significantly reduced collagen-type-II staining (p<0.01) associated with an increased MMP13 staining (p=0.07) was detected. The F-actin structure in cells isolated from PLS3 OE mice showed stress fiber formation at the cell edges compared to WT and Pls3 KO cells. Conclusion Articular cartilage homeostasis of 6-month-old female mice is influenced by PLS3 levels. Publication History Article published online: 18 October 2022 © 2022. Thieme. All rights reserved. Georg Thieme Verlag Rüdigerstraße 14, 70469 Stuttgart, Germany

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