Functional inhibition of the cardiac costamere induces the formation of contraction bands

收缩带(CB)坏死是心肌细胞单个肌节局部收缩所致，是缺血再灌注损伤的重要形态学标志。然而，CB的形成机制仍然不确定。我们假设局部消融β-dystroglan(β-DG)导致了消融部位的CBS的发生。为了解决这种可能性，我们将多光子(MP)激发诱发的CALI(Tanabe等人，NAT方法2005)应用于新生大鼠心脏，这些新生大鼠心脏编码与绿色荧光蛋白融合的蛋白质(βDG-EGFP)，其中绿色荧光蛋白荧光均匀分布在细胞膜上。MP刺激DG-EGFP在感兴趣区瞬间漂白EGFP，随后照射部位肌动蛋白细丝逐渐聚集，与CBS一致。总之，区域消融βDG导致CB的形成，这表明该蛋白在CBS的形成中起着重要作用。

Contraction band (CB) necrosis, a key morphological hallmark of ischemia-reperfusion injury, is caused by regional contracture at individual sarcomeres of cardiomyocytes. However, mechanisms for CB formation remain undetermined. We hypothesized that regional ablation of β-dystroglycan (βDG) leads to genesis of CBs at the ablated sites. To address this possibility, we applied multiphoton (MP) excitation-evoked CALI (Tanabe et al., Nat Methods 2005) to neonatal rat hearts transfected with cDNA encoding the protein fused with EGFP (βDG-EGFP), where EGFP fluorescence was homogeneously distributed along the cell membrane. MP-excitation of DG-EGFP at a localized area of interest resulted in instantaneous bleach of EGFP, followed by progressive and localized aggregation of actin filaments at the site of irradiation, consistent with CBs In summary, regional ablation of βDG resulted in formation of CB, suggesting an essential role of this protein in formation of CBs.