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Calcium-Sensing Receptor in Human Peripheral Blood T Lymphocytes Is Involved in the AMI Onset and Progression through the NF- κ B Signaling Pathway

View Article: PubMed Central - PubMed

ABSTRACT

Acute myocardial infarction (AMI) is a condition triggered by an inflammatory process that seriously affects human health. Calcium-sensing receptor (CaSR) in T lymphocytes is involved during the inflammation reaction. However, the relationship between them is not very clear. In this study, we collected human peripheral blood T lymphocytes from patients with AMI and in different stages of percutaneous coronary intervention (PCI) (at the onset of AMI, the first day after PCI (PCI-1), PCI-3, and PCI-5) to study the CaSR and NF-κB pathway protein expression, cytokine release and T cell apoptosis. The results showed that the expressions of CaSR, P-p65, Caspase-12, and the secretions of Th-1 and Th-2 type cytokines were increased at the onset of AMI, especially on the PCI-1. Meanwhile, the apoptosis rate of CD3+, CD4+ and CD8+ T lymphocytes also increased. However, from PCI-3, all the indicators began to decline. In addition, we also found that positive CaSR small interfering RNA (siRNA) transfection in T lymphocytes and NF-κB pathway blocker Bay-11-7082 reversed the increased expressions of CaSR, P-p65, Caspase-12, reduced the secretions of Th-1 and Th-2 type cytokines, and decreased T lymphocytes apoptosis rate not only in the AMI patients but also in the normal controls. All of these results indicated that CaSR in the human peripheral blood T lymphocytes were involved in the AMI onset and progression, which probably was related to the NF-κB pathway. Our study demonstrated the relationship between AMI and CaSR, and will provide new effective prevention theory and new targets for drug treatment.

No MeSH data available.


T cells apoptosis rate changed by CaSR siRNA transfection and Bay11-7082 (n = 20). The cell apoptosis rate was measured after T lymphocytes were transfected by CaSR siRNA plasmids for 24 h or were cultured by NF-κB pathway blocker Bay-11-7082 (10 mM) for 15 min. The apoptosis rate of all these T cells was quantified by densitometry. * p < 0.05 vs. Normal; □p < 0.05 vs. Normal + siRNA+; Δp < 0.05 vs. AMI; ◊p < 0.05 vs. AMI + siRNA+.
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ijms-17-01397-f006: T cells apoptosis rate changed by CaSR siRNA transfection and Bay11-7082 (n = 20). The cell apoptosis rate was measured after T lymphocytes were transfected by CaSR siRNA plasmids for 24 h or were cultured by NF-κB pathway blocker Bay-11-7082 (10 mM) for 15 min. The apoptosis rate of all these T cells was quantified by densitometry. * p < 0.05 vs. Normal; □p < 0.05 vs. Normal + siRNA+; Δp < 0.05 vs. AMI; ◊p < 0.05 vs. AMI + siRNA+.

Mentions: First, we found that the T lymphocytes apoptosis rate in the AMI group was higher than the normal group, and most of the apoptotic cells were in the later stage. Then, we noticed the CaSR siRNA positive- transfection inhibited the cell apoptosis not only in the AMI group but also in the normal group, and most of the apoptotic cells were in the early stage. Negative-transfection lymphocytes had no evident apoptosis appearing whether in the AMI or in the normal group. In addition, NF-κB pathway blocker Bay-11-7082 also decreased the apoptosis degree (p < 0.05) (Figure 6). This meant that CaSR and NF-κB pathways affected T lymphocytes apoptosis by interfering in the process of cell period cycle.


Calcium-Sensing Receptor in Human Peripheral Blood T Lymphocytes Is Involved in the AMI Onset and Progression through the NF- κ B Signaling Pathway
T cells apoptosis rate changed by CaSR siRNA transfection and Bay11-7082 (n = 20). The cell apoptosis rate was measured after T lymphocytes were transfected by CaSR siRNA plasmids for 24 h or were cultured by NF-κB pathway blocker Bay-11-7082 (10 mM) for 15 min. The apoptosis rate of all these T cells was quantified by densitometry. * p < 0.05 vs. Normal; □p < 0.05 vs. Normal + siRNA+; Δp < 0.05 vs. AMI; ◊p < 0.05 vs. AMI + siRNA+.
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Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC5037677&req=5

ijms-17-01397-f006: T cells apoptosis rate changed by CaSR siRNA transfection and Bay11-7082 (n = 20). The cell apoptosis rate was measured after T lymphocytes were transfected by CaSR siRNA plasmids for 24 h or were cultured by NF-κB pathway blocker Bay-11-7082 (10 mM) for 15 min. The apoptosis rate of all these T cells was quantified by densitometry. * p < 0.05 vs. Normal; □p < 0.05 vs. Normal + siRNA+; Δp < 0.05 vs. AMI; ◊p < 0.05 vs. AMI + siRNA+.
Mentions: First, we found that the T lymphocytes apoptosis rate in the AMI group was higher than the normal group, and most of the apoptotic cells were in the later stage. Then, we noticed the CaSR siRNA positive- transfection inhibited the cell apoptosis not only in the AMI group but also in the normal group, and most of the apoptotic cells were in the early stage. Negative-transfection lymphocytes had no evident apoptosis appearing whether in the AMI or in the normal group. In addition, NF-κB pathway blocker Bay-11-7082 also decreased the apoptosis degree (p < 0.05) (Figure 6). This meant that CaSR and NF-κB pathways affected T lymphocytes apoptosis by interfering in the process of cell period cycle.

View Article: PubMed Central - PubMed

ABSTRACT

Acute myocardial infarction (AMI) is a condition triggered by an inflammatory process that seriously affects human health. Calcium-sensing receptor (CaSR) in T lymphocytes is involved during the inflammation reaction. However, the relationship between them is not very clear. In this study, we collected human peripheral blood T lymphocytes from patients with AMI and in different stages of percutaneous coronary intervention (PCI) (at the onset of AMI, the first day after PCI (PCI-1), PCI-3, and PCI-5) to study the CaSR and NF-&kappa;B pathway protein expression, cytokine release and T cell apoptosis. The results showed that the expressions of CaSR, P-p65, Caspase-12, and the secretions of Th-1 and Th-2 type cytokines were increased at the onset of AMI, especially on the PCI-1. Meanwhile, the apoptosis rate of CD3+, CD4+ and CD8+ T lymphocytes also increased. However, from PCI-3, all the indicators began to decline. In addition, we also found that positive CaSR small interfering RNA (siRNA) transfection in T lymphocytes and NF-&kappa;B pathway blocker Bay-11-7082 reversed the increased expressions of CaSR, P-p65, Caspase-12, reduced the secretions of Th-1 and Th-2 type cytokines, and decreased T lymphocytes apoptosis rate not only in the AMI patients but also in the normal controls. All of these results indicated that CaSR in the human peripheral blood T lymphocytes were involved in the AMI onset and progression, which probably was related to the NF-&kappa;B pathway. Our study demonstrated the relationship between AMI and CaSR, and will provide new effective prevention theory and new targets for drug treatment.

No MeSH data available.