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Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication

Journal article
Authors Eva Skiöldebrand
Anna Thorfve
Ulrika Björklund
Pegah Johansson
Ruth Wickelgren
Anders Lindahl
Elisabeth Hansson
Published in Heliyon
Volume 4
Issue 1
ISSN 2405-8440
Publication year 2018
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Language en
Keywords Cell biology, central-nervous-system, human articular chondrocytes, evoked ca2+, transients, toll-like receptors, osteoarthritic-cartilage, ultralow, concentrations, functional expression, cultured astrocytes, gene-expression, calcium waves
Subject categories Cell biology, Neurosciences


Chondrocytes are effectively involved in the pathophysiological processes of inflammation in joints. They form cellular processes in the superficial layer of the articular cartilage and form gap junction coupled syncytium to facilitate cell-to-cell communication. However, very little is known about their physiological cellular identity and communication. The aim with the present work is to evaluate the physiological behavior after stimulation with the inflammatory inducers interleukin-1 beta and lipopolysaccharide. The cytoskeleton integrity and intracellular Ca2+ release were assessed as indicators of inflammatory state. Cytoskeleton integrity was analyzed through cartilage oligomeric matrix protein and actin labeling with an Alexa 488-conjugated phalloidin probe. Ca2+ responses were assessed through the Ca2+ sensitive fluorophore Fura-2/AM. Western blot analyses of several inflammatory markers were performed. The results show reorganization of the actin filaments. Glutamate, 5-hydoxytryptamine, and ATP evoked intracellular Ca2+ release changed from single peaks to oscillations after inflammatory induction in the chondrocytes. The expression of toll-like receptor 4, the glutamate transporters GLAST and GLT-1, and the matrix metalloproteinase-13 increased. This work demonstrates that chondrocytes are a key part in conditions that lead to inflammation in the cartilage. The inflammatory inducers modulate the cytoskeleton, the Ca2+ signaling, and several inflammatory parameters. In conclusion, our data show that the cellular responses to inflammatory insults from healthy and inflammatory chondrocytes resemble those previously observed in astrocyte and cardiac fibroblasts networks.

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Utskriftsdatum: 2019-12-13