Calcium‑sensing receptors in human peripheral T lymphocytes and AMI: Cause and effect.

Acute myocardial infarction (AMI) is a disease associated with inflammation. T lymphocytes are involved by secreting cytokines and inflammatory factors. In our previous study, it was found that the T lymphocytes exhibited certain functional changes, the onset of which was induced by modulating calcium‑sensing receptor (CaSR) in AMI. In the present study, western blotting was used to verified the expression of T lymphocyte CaSR and pathway proteins, including phosphorylated extracellular signal‑regulated kinase (P‑ERK)1/2 and phosphorylated c‑Jun N‑terminal kinase (P‑JNK), and used cytometric bead array to detect the secretion of interleukin (IL)‑4, IL‑6, IL‑10 and tumor necrosis factor (TNF)‑α in AMI onset, the results demonstrated that they were all increased. In addition, the expression of T lymphocyte pathway proteins, including P‑ERK1/2 and P‑JNK, and the secretion of IL‑4, IL‑6, IL‑10 and TNF‑α decreased after T lymphocytes being transfected by CaSR small interfering RNA. By contrast, the neonatal mouse cardiomyocytes under hypoxia and hypoxia/re‑oxygenation exhibited ultrastructural damage, increased apoptosis, increased production of lactate dehydrogenase (LDH) and malondialdehyde, and reduced superoxide dismutase; these indicators changed extensively when cardiomyocytes were co‑cultured with T lymphocytes. However, the effects were reversed when the cardiomyocytes were co‑cultured with CaSR‑silenced T lymphocytes. These results indicated that CaSR may modulate T lymphocytes to release cytokines through mitogen‑activated protein kinase pathways and affect cardiomyocyte injury. The relationship between AMI and T lymphocyte CaSR is reciprocal.