Alteration of serum and cardiac tissue adropin, copeptin, irisin and TRPM2 expressions in DOX treated male rats

Abstract

Doxorubicin (DOX) cardiotoxicity is a significant side effect in cancer survivors. DOX and its metabolites alter cardiac gene expression and affect metabolic energy-related peptides. Adropin, copeptin, irisin and TRPM2 are produced locally in the heart and play a role in energy homeostasis. We investigated the fates of adropin, copeptin, irisin and TRPM2 in serum and cardiac tissues of DOX treated rats. Animals were divided into three groups of six: 1) untreated controls, 2) DOX treated and 3) saline treated. The rats were fed a standard diet ad libitum for 14 days then were sacrificed and heart and serum samples were taken. Adropin, copeptin, irisin levels in tissue homogenates and serum were measured using ELISA. Immunoreactivity of heart tissue adropin, copeptin, irisin and TRPM2 also were investigated. The peptides increased in both serum and cardiac tissue homogenates in animals treated with DOX compared to the other groups. DOX increased adropin in endocardial and myocardial cells, but it decreased expression of copeptin. DOX did not affect endocardial irisin and TRPM2 expressions, but myocardial irisin and TRPM2 expressions were increased. Serum adropin, irisin and copeptin were increased in DOX treated rats. Cardiac adropin, copeptin, irisin and TRPM2 are affected by DOX and may play a role in DOX cardiotoxicity.

Irisin levels increase during experimentally induced acute myocardial infarction

“…In addition, a recent study by Aronis et al (16) noted that serum irisin levels had no predictive value in the development of acute coronary syndrome; however, increased irisin levels were related to the development of major adverse cardiac events after coronary intervention. Another study showed that in rats induced with cardiac toxicity using doxorubicin, myocardial and serum irisin levels were increased (17). This study had similarities with our study with respect to the increase observed in irisin level due to myocyte damage.…”

Effect of carnosine, methylprednisolone and their combined application on irisin levels in the plasma and brain of rats with acute spinal cord injury

“…Here our results show direct evidence that irisin is present in the brain and this is in agreement with previous observation (Dun et al, 2013), and spinal cord treatments with carnosine alone, MP alone or their combined application cause an increase in irisin expression in the brain tissues. Some other tissue irisin levels, like some other peptide hormones, have less in them than in their corresponding plasma Aydin et al, 2014a;Catak et al, 2014). We did not measure spinal cord tissues supernatant irisin level due to lack of sufficient tissue samples.…”

Both experimental hypothyroidism and hyperthyroidism increase cardiac irisin levels in rats

“…Group 1 (n = 8): Control: The rats in this group were sacrifi ced without being subjected to any procedure and the plasma obtained from their blood samples was stored at -80 °C until the time of analysis. Group 2 (n = 8): 6-n-propyl-2-thiouracil (PTU): To induce hypothyroidism, the rats in this group were administered 6-npropyl-2-thiouracil (10 mg/kg/day) by the intraperitoneal route daily for 3 weeks (10).…”

“…It has been also suggested that serum irisin and cardiovascular diseases might have a relationship (5,6,7,8,9). It has been reported that heart muscle had a high FNDC expression and production of irisin than skeletal muscle (10). Heart tissue irisin levels are reduced after the myocardial infarction and might be used as diagnostic agent.…”