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

Artikel i vetenskaplig tidskrift
Författare Eva Skiöldebrand
Anna Thorfve
Ulrika Björklund
Pegah Johansson
Ruth Wickelgren
Anders Lindahl
Elisabeth Hansson
Publicerad i Heliyon
Volym 4
Nummer/häfte 1
ISSN 2405-8440
Publiceringsår 2018
Publicerad vid Institutionen för biomedicin, avdelningen för klinisk kemi och transfusionsmedicin
Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap
Språk en
Länkar doi.org/10.1016/j.heliyon.2018.e005...
Ämnesord 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
Ämneskategorier Cellbiologi, Neurovetenskaper

Sammanfattning

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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Denna text är utskriven från följande webbsida:
http://www.gu.se/forskning/publikation/?publicationId=268260
Utskriftsdatum: 2019-09-19