Interaction between caspase‐3 and caspase‐5 in the stretch‐induced programmed cell death in the human periodontal ligament cells

2019 ◽  
Vol 234 (8) ◽  
pp. 13571-13581 ◽  
Author(s):  
Yaqin Wu ◽  
Jiabao Zhuang ◽  
Dan Zhao ◽  
Chun Xu
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Periodontal Ligament ◽  
Caspase 3 ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells

scholarly journals Knockdown of TRIM52 alleviates LPS-induced inflammatory injury in human periodontal ligament cells through the TLR4/NF-κB pathway

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Peng Liu ◽  
Lijun Cui ◽  
Lifang Shen
Keyword(s):  
Signaling Pathway ◽  
Periodontal Ligament ◽  
Caspase 3 ◽  
Quantitative Polymerase Chain Reaction ◽  
Periodontal Ligament Cells ◽  
Inflammatory Injury ◽  
Human Periodontal Ligament Cells ◽  
Diphenyltetrazolium Bromide ◽  
Tnf Α ◽  
Factor Α

Abstract Tripartite motif-containing (TRIM) 52 (TRIM52) is a vital regulator of inflammation. However, the function and mechanisms of TRIM52 in lipopolysaccharide (LPS)-induced inflammatory injury of human periodontal ligament cells (HPDLCs) in periodontitis remain undefined. In the present research, gene expression was determined using a quantitative polymerase chain reaction and Western blot. The effect of TRIM52 on LPS-induced inflammatory injury was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and enyzme-linked immunosorbent assay (ELISA). We found that TRIM52 expression was up-regulated in LPS-treated HPDLCs. Knockdown of TRIM52 alleviated LPS-induced proliferative inhibition and apoptosis promotion in HPDLCs, as evidenced by a decrease in cleaved caspase-3 expression and caspase-3 activity. Silencing TRIM52 suppressed LPS-induced inflammatory response of HPDLCs, as indicated by the decrease in interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α) levels, and increase in IL-10 levels. TRIM52 knockdown inhibited LPS-induced activation of TLR4/nuclear factor-κ B (NF-κB) signaling pathway. Taken together, knockdown of TRIM52 mitigated LPS-induced inflammatory injury via the TLR4/NF-κB signaling pathway, providing an effective therapeutic target for periodontitis.

scholarly journals Cell Death and Metabolic Stress in Gymnodinium catenatum Induced by Allelopathy

Toxins ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 506
Author(s):  
Leyberth José Fernández-Herrera ◽  
Christine Johanna Band-Schmidt ◽  
Tania Zenteno-Savín ◽  
Ignacio Leyva-Valencia ◽  
Claudia Judith Hernández-Guerrero ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Protein Content ◽  
Caspase 3 ◽  
Cellular Stress ◽  
Allelopathic Effect ◽  
Sod Activity ◽  
Free Media ◽  
O2 Production ◽  
Gymnodinium Catenatum

Allelopathy between phytoplankton species can promote cellular stress and programmed cell death (PCD). The raphidophyte Chattonella marina var. marina, and the dinoflagellates Margalefidinium polykrikoides and Gymnodinium impudicum have allelopathic effects on Gymnodinium catenatum; however, the physiological mechanisms are unknown. We evaluated whether the allelopathic effect promotes cellular stress and activates PCD in G. catenatum. Cultures of G. catenatum were exposed to cell-free media of C. marina var. marina, M. polykrikoides and G. impudicum. The mortality, superoxide radical (O2●−) production, thiobarbituric acid reactive substances (TBARS) levels, superoxide dismutase (SOD) activity, protein content, and caspase-3 activity were quantified. Mortality (between 57 and 79%) was registered in G. catenatum after exposure to cell-free media of the three species. The maximal O2●− production occurred with C. marina var. marina cell-free media. The highest TBARS levels and SOD activity in G. catenatum were recorded with cell-free media from G. impudicum. The highest protein content was recorded with cell-free media from M. polykrikoides. All cell-free media caused an increase in the activity of caspase-3. These results indicate that the allelopathic effect in G. catenatum promotes cell stress and caspase-3 activation, as a signal for the induction of programmed cell death.

GDNF From Human Periodontal Ligament Cells Treated With Pro-Inflammatory Cytokines Promotes Neurocytic Differentiation of PC12 Cells

2016 ◽  
Vol 118 (4) ◽  
pp. 699-708
Author(s):  
Shinichiro Yoshida ◽  
Naohide Yamamoto ◽  
Naohisa Wada ◽  
Atsushi Tomokiyo ◽  
Daigaku Hasegawa ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Pro Inflammatory Cytokines
Sign in / Sign up

Export Citation Format

Share Document