Atrial light chains (ALC1) are naturally present in adult heart atria, while ventricular light chains (VLC1) are predominant in ventricles. Degradation of VLC1 and re‑expression of ALC1 in heart ventricles are associated with heart disorders in response to pressure overload. The aim of the current study was to investigate changes in myosin light chain expression after simulated ischemia and simulated reperfusion (sI/sR). Human cardiomyocytes (HCM) isolated from adult heart ventricles were subjected to chemical ischemia. The control group was maintained under aerobic conditions. Myocyte injury was determined by testing lactate dehydrogenase (LDH) activity. The gene expression of ALC1, VLC1 and MMP‑2 were assessed by reverse transcription‑quatitive PCR. Additionally, protein synthesis was measured using ELISA kits and MMP‑2 activity was measured by zymography. The results revealed that LDH activity was increased in sI/sR cell‑conditioned medium (P=0.02), confirming the ischemic damage of HCM. ALC1 gene expression and content in HCM were also increased in the sI/sR group (P=0.03 and P<0.001, respectively), while VLC1 gene expression after sI/sR was decreased (P=0.008). Furthermore, MMP‑2 gene expression and synthesis were lower in the sI/sR group when compared with the aerobic control group (P<0.001 and P=0.03, respectively). MMP‑2 activity was also increased in sI/sR cell‑conditioned medium (P=0.006). In conclusion, sI/sR treatment led to increased ALC1 and decreased VLC1 expression in ventricular cardiomyocytes, which may constitute an adaptive mechanism to altered conditions and contribute to the improvement of heart function.

中文翻译：

---

化学缺血再灌注损伤后培养的人心肌细胞中心房胎儿轻链的表达。

心房轻链 (ALC1) 天然存在于成人心房中，而心室轻链 (VLC1) 主要存在于心室中。心室中 VLC1 的降解和 ALC1 的重新表达与压力过载引起的心脏疾病有关。本研究的目的是研究模拟缺血和模拟再灌注 (sI/sR) 后肌球蛋白轻链表达的变化。从成人心室分离的人心肌细胞 (HCM) 受到化学缺血。对照组维持在有氧条件下。通过测试乳酸脱氢酶 (LDH) 活性来确定肌细胞损伤。通过逆转录定量 PCR 评估 ALC1、VLC1 和 MMP-2 的基因表达。此外，使用 ELISA 试剂盒测量蛋白质合成，并通过酶谱法测量 MMP-2 活性。结果显示，sI/sR细胞条件培养基中LDH活性增加（P=0.02），证实了HCM的缺血性损伤。sI/sR组中ALC1基因表达和HCM含量也增加（分别为P=0.03和P<0.001），而sI/sR后VLC1基因表达减少（P=0.008）。此外，与有氧对照组相比，sI/sR组的MMP-2基因表达和合成较低（分别为P<0.001和P=0.03）。MMP-2 活性在 sI/sR 细胞条件培养基中也有所增加（P=0.006）。总之，sI/sR 治疗导致心室心肌细胞中 ALC1 增加和 VLC1 表达降低，