Tetradecylthioacetic acid modulates cardiac transcription in Atlantic salmon, Salmo salar L., suffering heart and skeletal muscle inflammation

Abstract

Heart and skeletal muscle inflammation (HSMI) is a disease causing considerable mortality in farmed Atlantic salmon. We have previously reported that pre-feeding of tetradecylthioacetic acid (TTA) reduces the mortality during a natural outbreak of HSMI. In the present paper we show that in the cardiac ventricle, during HSMI infection, pre-feeding TTA increases the expression of the immune genes: TNFα, VCAM-1, IgM and CD8α. We also show that TTA increases the cardiosomatic index potentially by elevating cardiomyogenesis through activation of the cardiac transcription factors MEF2C and Nkx2.5. Using the recently published genomic sequence of a HSMI associated piscine reovirus (PRV), we could show that the PRV levels have no confounding effects on the mRNA expression of the investigated genes. The results suggest that TTA induced cardiac growth, together with an elevated cardiac recruitment of immune cells, which might lead to increased robustness during HSMI infection.

Cardiac pathological changes of Atlantic salmon (Salmo salar L.) affected with heart and skeletal muscle inflammation (HSMI)

“…It reflected that the inflammatory response was not primarily comprised of granulocytes in HSMI affected hearts. TUNEL identified nonesignificant moderate levels of staining for apoptotic cells in diseased hearts while caspase 3 presented with low levels of staining in the diseased hearts due to the fact that HSMI is a disease of more inflammation than necrosis/ apoptosis [2,3,8] and in line with Grammes et al [55]. Western blot analysis confirmed the specificity of caspase 3 antibody and identified procaspase 3 (w40 kDa) and caspase 3 (w12 kDa) bands and in line with Chiou et al [56] while the middle bands (w21 kDa) may correspond to the p20 that is formed by the cleavage of procaspase 3 to caspase 3 in mammals [57].…”

Genome wide response to dietary tetradecylthioacetic acid supplementation in the heart of Atlantic Salmon (Salmo salar L)

“…It should also be noted that although we did not find significant differences in relative heart weight in this study, in other studies we found that TTA significantly increases heart size in Atlantic salmon [8,9], and that the effect seems to be correlated to the dose of TTA (Rørvik, unpublished data). Thus, it is tempting to speculate that the increase in relative heart weight may be related to the cardiac transcriptional changes induced by TTA.…”

“…Previous results also suggested that TTA stimulates the transcription of PPAR α and β in the heart [8,9], thus indicating that TTA affects the metabolism in Atlantic salmon through activation of PPARs, similar to the mechanism known from rodents. Interestingly, this activation of PPARs may have been related to increased survival after a natural outbreak of a heart related viral disease in Atlantic salmon [8,9]. In mammals, cardiac activation of PPARs has yielded substantial attention due to the fact that PPARs have been proven to be major regulators of cardiac metabolism [10-13].…”

“…Furthermore, TTA reduces the secretion of triacylglycerides from Atlantic salmon hepatocytes in vitro [7] and has been shown to increase the expression of genes associated with fat metabolism in the liver and the heart ventricle [1,8]. Previous results also suggested that TTA stimulates the transcription of PPAR α and β in the heart [8,9], thus indicating that TTA affects the metabolism in Atlantic salmon through activation of PPARs, similar to the mechanism known from rodents. Interestingly, this activation of PPARs may have been related to increased survival after a natural outbreak of a heart related viral disease in Atlantic salmon [8,9].…”

Comparative cardiac pathological changes of Atlantic salmon (Salmo salar L.) affected with heart and skeletal muscle inflammation (HSMI), cardiomyopathy syndrome (CMS) and pancreas disease (PD)

“…(1997). The CMS and PD are the cardiac diseases identified with more degenerative changes as compared to HSMI where inflammatory changes dominated in the heart (Kongtorp et al, 2004(Kongtorp et al, , 2004aGrammes et al 2012). These findings were pointing the high cell turn over in the hearts where DNA damage/repair might be the case (as identified by PCNA, caspase 3 and TUNEL reactivity) (Table 2) (Ferguson et al, 1986;Poppe and Ferguson, 2006;Kongtorp et al, 2004Kongtorp et al, , 2006.…”