Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion.

ABSTRACT:

Aims

Junctin and triadin are calsequestrin-binding proteins that regulate sarcoplasmic reticulum (SR) Ca(2+) release by interacting with the ryanodine receptor. The levels of these proteins are significantly down-regulated in failing human hearts. However, the significance of such decreases is currently unknown. Here, we addressed the functional role of these accessory proteins in the heart's responses to ischaemia/reperfusion (I/R) injury.

Methods and results

Isolated mouse hearts were subjected to global I/R, and contractile parameters were assessed in wild-type (WT), junctin-knockout (JKO), and triadin-knockout (TKO) hearts. Both JKO and TKO were associated with significantly depressed post-I/R contractile recovery. However, ablation of triadin resulted in the most severe

SUBMITTER: Cai WF 

PROVIDER: S-EPMC3331615 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature