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Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells
Background Rotator cuff tears are a common cause of shoulder pain and impairment. Subacromial glucocorticoid injections are widely used for treatment of epiphenomenons of chronic impingement syndrome with the possible side effects of tendon rupture and impaired tendon healing. Methods Using qRT-PCR,...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Informa Healthcare
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823208/ https://www.ncbi.nlm.nih.gov/pubmed/19421912 http://dx.doi.org/10.3109/17453670902988360 |
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author | Tempfer, Herbert Gehwolf, Renate Lehner, Christine Wagner, Andrea Mtsariashvili, Maia Bauer, Hans-Christian Resch, Herbert Tauber, Mark |
author_facet | Tempfer, Herbert Gehwolf, Renate Lehner, Christine Wagner, Andrea Mtsariashvili, Maia Bauer, Hans-Christian Resch, Herbert Tauber, Mark |
author_sort | Tempfer, Herbert |
collection | PubMed |
description | Background Rotator cuff tears are a common cause of shoulder pain and impairment. Subacromial glucocorticoid injections are widely used for treatment of epiphenomenons of chronic impingement syndrome with the possible side effects of tendon rupture and impaired tendon healing. Methods Using qRT-PCR, western blot, immunoflourescence, and measurement of (3)H-thymidine uptake we investigated the effects of the crystalline glucocorticoid triamcinolone acetonide (TAA) when added to the culture medium of isolated human rotator cuff tendon cells. Results After 2 weeks of incubation, the cells had lost their fibroblastic appearance and parallel orientation, which is characteristic of cellular degeneration in vivo. Moreover, expression and secretion of collagen I was strongly reduced, and there was a decrease in proliferation rate. Cell migration was blocked and the rate of expression of the matrix metalloproteinases MMP2, MMP8, MMP9, and MMP13 was reduced, but expression of TIMP1 (a tissue inhibitor of MMPs) was upregulated, indicating a reduction in the cellular capacity for tendon repair. In addition, changes in cellular differentiation were observed: the number of adipocytes increased and levels of the protein Sox9—a marker of differentiating and mature chondrocytes—were elevated in triamcinolone acetonide treated cells. Interpretation These results may indicate that the use of TAA is one reason for weaker mechanical tendon properties and for the high rate of re-rupture after supraspinatus tendon repair. |
format | Text |
id | pubmed-2823208 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Informa Healthcare |
record_format | MEDLINE/PubMed |
spelling | pubmed-28232082010-02-18 Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells Tempfer, Herbert Gehwolf, Renate Lehner, Christine Wagner, Andrea Mtsariashvili, Maia Bauer, Hans-Christian Resch, Herbert Tauber, Mark Acta Orthop Research Article Background Rotator cuff tears are a common cause of shoulder pain and impairment. Subacromial glucocorticoid injections are widely used for treatment of epiphenomenons of chronic impingement syndrome with the possible side effects of tendon rupture and impaired tendon healing. Methods Using qRT-PCR, western blot, immunoflourescence, and measurement of (3)H-thymidine uptake we investigated the effects of the crystalline glucocorticoid triamcinolone acetonide (TAA) when added to the culture medium of isolated human rotator cuff tendon cells. Results After 2 weeks of incubation, the cells had lost their fibroblastic appearance and parallel orientation, which is characteristic of cellular degeneration in vivo. Moreover, expression and secretion of collagen I was strongly reduced, and there was a decrease in proliferation rate. Cell migration was blocked and the rate of expression of the matrix metalloproteinases MMP2, MMP8, MMP9, and MMP13 was reduced, but expression of TIMP1 (a tissue inhibitor of MMPs) was upregulated, indicating a reduction in the cellular capacity for tendon repair. In addition, changes in cellular differentiation were observed: the number of adipocytes increased and levels of the protein Sox9—a marker of differentiating and mature chondrocytes—were elevated in triamcinolone acetonide treated cells. Interpretation These results may indicate that the use of TAA is one reason for weaker mechanical tendon properties and for the high rate of re-rupture after supraspinatus tendon repair. Informa Healthcare 2009-06-05 2009-06-01 /pmc/articles/PMC2823208/ /pubmed/19421912 http://dx.doi.org/10.3109/17453670902988360 Text en Copyright: © Nordic Orthopedic Federation http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited. |
spellingShingle | Research Article Tempfer, Herbert Gehwolf, Renate Lehner, Christine Wagner, Andrea Mtsariashvili, Maia Bauer, Hans-Christian Resch, Herbert Tauber, Mark Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
title | Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
title_full | Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
title_fullStr | Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
title_full_unstemmed | Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
title_short | Effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
title_sort | effects of crystalline glucocorticoid triamcinolone acetonide on cultered human supraspinatus tendon cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823208/ https://www.ncbi.nlm.nih.gov/pubmed/19421912 http://dx.doi.org/10.3109/17453670902988360 |
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