Abstract
ABSTRACTThe form and function of the rainbow trout heart can remodel in response to various stressors including changes in environmental temperature and anemia. 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 signaling 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 24 h 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 mechanotransductive pathways are active in cardiac fibroblasts, and lead to the activation of cell signaling pathways involved in cardiac remodeling.
Highlights
The fish heart has a significant capacity to remodel in response to changes in physiological conditions (Alderman et al, 2012; Johnson et al, 2014; Keen et al, 2016; Klaiman et al, 2011; Marques et al, 2008; Simonot and Farrell, 2007)
Cold acclimation causes an increase in deposited collagen in the extracellular matrix (ECM) of the rainbow trout myocardium (Keen et al, 2016; Klaiman et al, 2011)
There was no difference in the levels of total p38 mitogen activated protein kinase (MAPK) or ERK protein between control and the treatment timepoints (P>0.05); there was a 4.2-fold increase in p38 MAPK phosphorylation after 20 min of 10% equibiaxial deformation (Fig. 1)
Summary
The fish heart has a significant capacity to remodel in response to changes in physiological conditions (Alderman et al, 2012; Johnson et al, 2014; Keen et al, 2016; Klaiman et al, 2011; Marques et al, 2008; Simonot and Farrell, 2007). Cold acclimation causes an increase in deposited collagen in the extracellular matrix (ECM) of the rainbow trout myocardium (Keen et al, 2016; Klaiman et al, 2011) This is interesting because a significant increase in collagen deposition in the mammalian heart is associated with a pathological condition that is permanent and results in diastolic dysfunction.
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