ArticleJournal of tissue engineering and regenerative medicine2015
ERK activation is required for hydrostatic pressure-induced tensile changes in engineered articular cartilage.
Article in Journal of tissue engineering and regenerative medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Minipig costal and knee cartilage structure-function relationships and their use as cell sources for tissue-engineered analogous cellular products for cartilage repair.Acta biomaterialia · 2026Article
- Articular cartilage tissue engineering: the role of signaling molecules.Cellular and molecular life sciences : CMLS · 2016Review
- Inducing articular cartilage phenotype in costochondral cells.Arthritis research & therapy · 2013Article
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2 authors.
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Abstract
The objective of this study was to identify ERK 1/2 involvement in the changes in compressive and tensile mechanical properties associated with hydrostatic pressure treatment of self-assembled cartilage constructs. In study 1, ERK 1/2 phosphorylation was detected by immunoblot, following application of hydrostatic pressure (1 h of static 10 MPa) applied at days 10-14 of self-assembly culture. In study 2, ERK 1/2 activation was blocked during hydrostatic pressure application on days 10-14. With pharmacological inhibition of the ERK pathway by the MEK1/ERK inhibitor U0126 during hydrostatic pressure application on days 10-14, the increase in Young's modulus induced by hydrostatic pressure was blocked. Furthermore, this reduction in Young's modulus with U0126 treatment during hydrostatic pressure application corresponded to a decrease in total collagen expression. However, U0126 did not inhibit the increase in aggregate modulus or GAG induced by hydrostatic pressure. These findings demonstrate a link between hydrostatic pressure application, ERK signalling and changes in the biomechanical properties of a tissue-engineered construct.
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