Enhanced N-terminal degradation of troponin I blunts cardiac function responsiveness to isoproterenol in 4-week tail-suspended rats

  • Authors:
    • Lin Zhang
    • Zhen Song
    • Hui Chang
    • Yun-Ying Wang
    • Zhi-Bin Yu
  • View Affiliations

  • Published online on: October 8, 2012     https://doi.org/10.3892/mmr.2012.1119
  • Pages: 271-279
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The N-terminal extension of cardiac troponin I (cTnI) is important in regulating cardiac function. Although the normal rat myocardium shows some cTnI N-terminal degradation (cTnI-ND), exposure to 4 weeks of tail-suspension markedly increased cTnI-ND. We hypothesized that the increased cTnI-ND in tail-suspended rats may affect cardiac function, particularly during β-adrenergic (β-A) stimulation. The increase in cardiac output with isoproterenol (ISO) treatment was smaller in tail-suspended rats compared with controls. Left ventricular end-diastolic pressure was elevated and increases in maximal rates of left ventricular pressure development and relaxation were lower during ISO treatment in tail-suspended rats. Response to ISO, forskolin, DB-cAMP and IBMX was also lower in cardiomyocytes from tail-suspended rats. The increase in shortening and re-lengthening the rates of cardiomyocytes at a maximal dose of ISO, forskolin, DB-cAMP and IBMX treatment was limited in tail-suspended rats. There was no difference in Ca2+ sensitivity of the isometric force between tail-suspended and control rats, although Ca2+ sensitivity was decreased less in tail-suspended rats versus control rats during PKA phosphorylation. There was no difference in PKA protein expression and activation during ISO stimulation between the two groups. Due to the increase in cTnI-ND, ISO-induced phosphorylation of cTnI was reduced in tail-suspended rats. The total phospholamban expression and phosphorylation by ISO was unaltered in tail-suspended rat hearts. These data suggest that enhanced cTnI-ND following 4-week tail-suspension is a major component of the β-A receptor signaling pathway, depressing cardiac function under ISO stimulation.
View Figures
View References

Related Articles

Journal Cover

January 2013
Volume 7 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang L, Song Z, Chang H, Wang Y and Yu Z: Enhanced N-terminal degradation of troponin I blunts cardiac function responsiveness to isoproterenol in 4-week tail-suspended rats. Mol Med Rep 7: 271-279, 2013
APA
Zhang, L., Song, Z., Chang, H., Wang, Y., & Yu, Z. (2013). Enhanced N-terminal degradation of troponin I blunts cardiac function responsiveness to isoproterenol in 4-week tail-suspended rats. Molecular Medicine Reports, 7, 271-279. https://doi.org/10.3892/mmr.2012.1119
MLA
Zhang, L., Song, Z., Chang, H., Wang, Y., Yu, Z."Enhanced N-terminal degradation of troponin I blunts cardiac function responsiveness to isoproterenol in 4-week tail-suspended rats". Molecular Medicine Reports 7.1 (2013): 271-279.
Chicago
Zhang, L., Song, Z., Chang, H., Wang, Y., Yu, Z."Enhanced N-terminal degradation of troponin I blunts cardiac function responsiveness to isoproterenol in 4-week tail-suspended rats". Molecular Medicine Reports 7, no. 1 (2013): 271-279. https://doi.org/10.3892/mmr.2012.1119