Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication
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...
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2018-01-01
|
| Series: | Heliyon |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844017327068 |
| _version_ | 1818839068552724480 |
|---|---|
| author | Eva Skiöldebrand Anna Thorfve Ulrika Björklund Pegah Johansson Ruth Wickelgren Anders Lindahl Elisabeth Hansson |
| author_facet | Eva Skiöldebrand Anna Thorfve Ulrika Björklund Pegah Johansson Ruth Wickelgren Anders Lindahl Elisabeth Hansson |
| author_sort | Eva Skiöldebrand |
| collection | DOAJ |
| description | 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-1β 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. |
| first_indexed | 2024-12-19T03:48:25Z |
| format | Article |
| id | doaj.art-88fd13edf34043798d967cb0dd361b66 |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-12-19T03:48:25Z |
| publishDate | 2018-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-88fd13edf34043798d967cb0dd361b662022-12-21T20:37:03ZengElsevierHeliyon2405-84402018-01-014110.1016/j.heliyon.2018.e00525Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communicationEva Skiöldebrand0Anna Thorfve1Ulrika Björklund2Pegah Johansson3Ruth Wickelgren4Anders Lindahl5Elisabeth Hansson6Department of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, SwedenDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, SwedenDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, SwedenDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, SwedenDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, SwedenDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, SwedenDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, SwedenChondrocytes 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-1β 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.http://www.sciencedirect.com/science/article/pii/S2405844017327068Cell biology |
| spellingShingle | Eva Skiöldebrand Anna Thorfve Ulrika Björklund Pegah Johansson Ruth Wickelgren Anders Lindahl Elisabeth Hansson Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication Heliyon Cell biology |
| title | Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication |
| title_full | Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication |
| title_fullStr | Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication |
| title_full_unstemmed | Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication |
| title_short | Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication |
| title_sort | biochemical alterations in inflammatory reactive chondrocytes evidence for intercellular network communication |
| topic | Cell biology |
| url | http://www.sciencedirect.com/science/article/pii/S2405844017327068 |
| work_keys_str_mv | AT evaskioldebrand biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication AT annathorfve biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication AT ulrikabjorklund biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication AT pegahjohansson biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication AT ruthwickelgren biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication AT anderslindahl biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication AT elisabethhansson biochemicalalterationsininflammatoryreactivechondrocytesevidenceforintercellularnetworkcommunication |