Publication: Latexin expression correlated with mineralization of articular cartilage during progression of post-traumatic osteoarthritis in a rat model
Authors
Martínez Calleja, América ; Cruz, Raymundo ; Miranda Sánchez, Magdalena ; Fragoso Soriano, Rogelio ; Vega López, Marco A. ; Kour, Juan B.
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-151
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info:eu-repo/semantics/article
Description
Abstract
As latexin has been linked with chondrocyte
hypertrophic differentiation it is possible that this protein
may also be involved in the mineralization of cartilage in
OA. Therefore, we correlated latexin expression with the
mineralization marker, alkaline phosphatase and
determined the mineral deposition in the articular
cartilage by analyzing the Ca/P ratio and the collagen
fibrils pattern, during the progression of post-traumatic
OA in a rat model. OA was induced by medial
meniscectomy and post-surgery exercise for 5, 10, 20
and 45 days. Protein expression in articular cartilage was
evaluated by immunofluorescence, histochemistry and
Western blot. Minerals and structure of collagen fibrils
in the superficial zone of cartilage were analyzed by
energy dispersive X-ray spectroscopy (EDX) and atomic
force microscopy (AFM) respectively. Protein
expression analysis showed time-dependent up-
regulation of latexin during OA progression. In the
cartilage, latexin expression correlated with the
expression and activity of alkaline phosphatase. EDX of
the superficial zone of cartilage showed a Ca/P ratio
closer to theoretical values for basic calcium phosphate
minerals. The presence of minerals was also analyzed
indirectly with AFM, as the collagen fibril pattern was
less evident in the mineralized tissue. Latexin is
expressed in articular cartilage from the early stages of
post-traumatic OA; however, minerals were detected
after latexin expression was up-regulated, indicating that
its activity precedes and remains during the pathological
mineralization of cartilage. Thus, our results contribute
to the identification of molecules involved in the
mineralization of articular chondrocytes.
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Citation
Histology and Histopathology Vol. 35, nº 3 (2020)
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