Vibration activates the actin/NF‐κB axis and upregulates IL‐6 and IL‐8 expression in human periodontal ligament cells

Abstract

We previously reported that mechanical vibration‐induced proinflammatory cytokines, interleukin‐6 (IL‐6) and IL‐8, expression in human periodontal ligament (hPDL) cells, however, the underlying mechanism remained unclear. Mechanical stimuli are able to activate cellular responses by inducing the activation of several signaling pathways including cytoskeletal changes and inflammation. The actin cytoskeleton is a highly dynamic network and plays many important roles in intracellular events. Here, we aimed to investigate the involvement of a pivotal mediator of inflammatory responses, nuclear factor‐κB (NF‐κB), and actin polymerization in vibration‐induced upregulation of IL‐6 and IL‐8 expression in hPDL cells. hPDL cells were pretreated with the NF‐κB inhibitor BAY 11‐7082 or cytochalasin D, respectively, before exposure to vibration. IL‐6 and IL‐8 messenger RNA (mRNA) and protein expression were quantified by quantitative polymerase chain reaction and enzyme‐linked immunosorbent assays, respectively. Subcellular localization of the NF‐κB p65 subunit was visualized by immunofluorescent staining. We found an increase in NF‐κB nuclear translocation in vibrated cells compared with control cells. Pretreatment with BAY 11‐7082 significantly inhibited vibration‐induced IL‐6 and IL‐8 mRNA and protein expression in hPDL cells. Moreover, pretreatment with cytochalasin D inhibited NF‐κB nuclear translocation and attenuated upregulation of IL‐6 and IL‐8 mRNA and protein in vibrated cells. Therefore, modulation of actin cytoskeletal polymerization in response to vibration may activate the NF‐κB signaling pathway and subsequently upregulate IL‐6 and IL‐8 expression in hPDL cells.

Cyclic tensile strain affects the response of human periodontal ligament stromal cells to tumor necrosis factor-α

“…For example, the application of CTS with 10% elongation and a frequency of 1 Hz yielded an increased the level of IL-6 in primary human PDL cells within the first 2- or 6 h of strain [ 48 ]. Similar observations with an increased IL-6 have been made with the application of static tension [ 57 ], hydrostatic pressure (HP) [ 26 ], or vibration with 30 Hz [ 63 ]. Moreover, IL-8 expression was up-regulated under the application of 3 ~ 15% cyclic stretching with a frequency of 0.2 Hz after 24 h [ 49 ].…”

HRG inhibits liver cancer lung metastasis by suppressing neutrophil extracellular trap formation

“…Studies 19,20 have found that FCγR1 maintains the activated state of neutrophils by PI3K after binding to the immune complex. In addition, IL‐8 is also a downstream target for the known PI3K‐NF‐κB signalling pathway, 21–23 and we found that HRG inhibits the conduction of the PI3K and NF‐κB signalling pathways and reduces the production of downstream IL‐8. We found that the use of anti‐FCγR1 antibody eliminated the effects of HRG on the PI3K and NF‐κB signalling pathways and IL‐8 (Figures 4G and H), further demonstrating that HRG inhibits PI3K and the NF‐κB signalling pathway by binding to the FCγR1 receptor and thus affects neutrophil chemotaxis.…”

Actin-Binding Proteins as Potential Biomarkers for Chronic Inflammation-Induced Cancer Diagnosis and Therapy

“…ABPs help regulate the actin skeleton polymerization. This modulation can [64]. For example, Arp2/3 complex-dependent actin skeleton remodeling is important for B cell activation to alleviate inflammatory responses [65].…”

“…ABPs help regulate the actin skeleton polymerization. This modulation can activate inflammation-related NF- κ B signaling pathways and subsequently upregulate the expression of IL-6 and IL-8 in inflammatory diseases, such as periodontal ligament tissue inflammation [ 64 ]. For example, Arp2/3 complex-dependent actin skeleton remodeling is important for B cell activation to alleviate inflammatory responses [ 65 ].…”