Key result
Cyclical stretch of trout cardiac fibroblasts elevated p38 MAPK phosphorylation by 4.2-fold at 20 minutes and ERK1/2 phosphorylation by 2.4-fold at 24 hours compared to control cells (P<0.05).
Why the study?
The influence of biomechanical forces on trout myocardium and the cellular signals translating such stimuli into cardiac remodeling responses have not been examined.
Does cyclical stretch activate MAPK signaling pathways in cultured rainbow trout cardiac fibroblasts?
Does cyclical stretch activate MAPK signaling pathways in cultured rainbow trout cardiac fibroblasts?
Effect estimate: 4.2-fold increase (p38 at 20 min); 2.4-fold increase (ERK1/2 at 24h)
p-value: p=<0.05
Biomechanical forces (cyclical stretch) activate mechanotransducive MAPK signaling pathways in trout cardiac fibroblasts, suggesting a mechanism for cardiac remodeling in response to physiological stressors.
No clinical implications from trout cell data; leaves open cross-species conservation of stretch-induced cardiac fibroblast signaling.
The form and function of the rainbow trout heart can remodel in response to various stressors including changes in environmental temperature and anaemia. Previous studies have hypothesized that changes in biomechanical forces experienced by the trout myocardium as result of such physiological stressors could play a role in triggering the remodeling response. However, there has been no work examining the influence of biomechanical forces on the trout myocardium or of the cellular signals that would translate such a stimuli into a biological response. In this study, we test the hypothesis that the application of biomechanical forces to trout cardiac fibroblasts activate the cell signalling pathways associated with cardiac remodeling. This was done by cyclically stretching cardiac fibroblasts to 10% equibiaxial deformation at 0.33 Hz and quantifying the activation of the p38-JNK-ERK mitogen activated protein kinase (MAPK) pathway. After 20 min, p38 MAPK phosphorylation was elevated by 4.2-fold compared to control cells (P<0.05) and after 24h of stretch, p38 MAPK phosphorylation remained elevated and extracellular-regulated kinase 1/2 was phosphorylated by 2.4-fold compared to control (P<0.05). Together, these results indicate that mechanotransducive pathways are active in cardiac fibroblasts, and lead to the activation of cell signalling pathways involved in cardiac remodeling.
No takes yet. Share an insight, caveat, or question.
Johnston et al. (2019) studied Cultured fibroblasts from rainbow trout hearts. Cyclical stretch vs. Control cells was evaluated on Activation of the p38-JNK-ERK mitogen activated protein kinase (MAPK) pathway (4.2-fold increase (p38 at 20 min); 2.4-fold increase (ERK1/2 at 24h), p=<0.05). Cyclical stretch of trout cardiac fibroblasts elevated p38 MAPK phosphorylation by 4.2-fold at 20 minutes and ERK1/2 phosphorylation by 2.4-fold at 24 hours compared to control cells (P<0.05).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: