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首页> 外文期刊>Cellular Physiology and Biochemistry >Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells
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Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells

机译：钙/钙调蛋白依赖性蛋白激酶IV介导IFN-γ诱导的骨骼肌细胞免疫行为。

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Background/Aims Whether calcium/calmodulin-dependent protein kinase IV (CaMKIV) plays a role in regulating immunologic features of muscle cells in inflammatory environment, as it does for immune cells, remains mostly unknown. In this study, we investigated the influence of endogenous CaMKIV on the immunological characteristics of myoblasts and myotubes received IFN-γ stimulation. Methods C2C12 and murine myogenic precursor cells (MPCs) were cultured and differentiated in vitro, in the presence of pro-inflammatory IFN-γ. CaMKIV shRNA lentivirus transfection was performed to knockdown CaMKIV gene in C2C12 cells. pEGFP-N1-CaMKIV plasmid was delivered into knockout cells for recovering intracellular CaMKIV gene level. CREB1 antagonist KG-501 was used to block CREB signal. qPCR, immunoblot analysis, or immunofluorescence was used to detect mRNA and protein levels of CaMKIV, immuno-molecules, or pro-inflammatory cytokines and chemokines. Co-stimulatory molecules expression was assessed by FACS analysis. Results IFN-γ induces the expression or up-regulation of MHC-I/II and TLR3, and the up-regulation of CaMKIV level in muscle cells. In contrast, CaMKIV knockdown in myoblasts and myotubes leads to expression inhibition of the above immuno-molecules. As well, CaMKIV knockdown selectively inhibits pro-inflammatory cytokines/chemokines, and co-stimulatory molecules expression in IFN-γ treated myoblasts and myotubes. Finally, CaMKIV knockdown abolishes IFN-γ induced CREB pathway molecules accumulation in differentiated myotubes. Conclusions CaMKIV can be induced to up-regulate in muscle cells under inflammatory condition, and positively mediates intrinsic immune behaviors of muscle cells triggered by IFN-γ.
机译：背景/目的钙/钙调蛋白依赖性蛋白激酶IV（CaMKIV）是否像炎症细胞一样在炎性环境中调节肌肉细胞的免疫学特征是否起作用，仍然未知。在这项研究中，我们调查了内源性CaMKIV对成肌细胞和接受IFN-γ刺激的肌管的免疫学特征的影响。方法在促炎性IFN-γ存在下，体外培养和分化C2C12和鼠肌原代细胞（MPCs）。进行CaMKIV shRNA慢病毒转染以敲低C2C12细胞中的CaMKIV基因。将pEGFP-N1-CaMKIV质粒递送至敲除细胞中以恢复细胞内CaMKIV基因水平。 CREB1拮抗剂KG-501用于阻断CREB信号。使用qPCR，免疫印迹分析或免疫荧光检测CaMKIV，免疫分子或促炎细胞因子和趋化因子的mRNA和蛋白水平。通过FACS分析评估共刺激分子表达。结果IFN-γ诱导肌肉细胞中MHC-I / II和TLR3的表达或上调，以及CaMKIV水平的上调。相反，在成肌细胞和肌管中的CaMKIV敲低导致上述免疫分子的表达抑制。同样，CaMKIV敲低选择性抑制促炎细胞因子/趋化因子，并在IFN-γ处理的成肌细胞和成肌细胞中共刺激分子表达。最终，CaMKIV敲除消除了IFN-γ诱导的CREB途径分子在分化肌管中的积累。结论CaMKIV在炎性条件下可诱导肌细胞上调，并积极介导IFN-γ触发的肌细胞内在免疫行为。

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