NDLI: Inhibition of granzyme B activity blocks inflammation induced by lipopolysaccharide through regulation of endoplasmic reticulum stress signaling in NK92 cells.

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Inhibition of granzyme B activity blocks inflammation induced by lipopolysaccharide through regulation of endoplasmic reticulum stress signaling in NK92 cells.

Content Provider	Semantic Scholar
Author	Wang, Lei Jiang, Shaowei Xiao, Ling Chen, Lin Zhang, Yanyan Tong, Jing
Copyright Year	2018
Abstract	Granzyme B (GrB) is a serine protease that is expressed in the lytic granules of natural killer (NK) cells and cytotoxic T lymphocytes (CTL), and which has been widely reported to serve a crucial role for target cell apoptosis. GrB may serve a non‑cytotoxic role in inflammation, but the evidence remains unclear. The present study aimed to establish an inflammatory cell model by using NK92 cells stimulated with lipopolysaccharide (LPS) to investigate whether GrB was involved in the development of inflammation. The extracellular levels of tumor necrosis factor‑α (TNF‑α), interleukin‑1β (IL‑1β) and GrB were examined by ELISA, and it was demonstrated that LPS treatment increased the extracellular levels of TNF‑α, IL‑1β and GrB, and these increased expression levels were inhibited by pretreatment with the GrB inhibitor serpin A3N (SA3N). The protein expression levels of glucose‑regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), nuclear factor‑κB (NF‑κB), inhibitor of NF‑κB (IκBα) and GrB were examined by western blot analysis. The results demonstrated that LPS stimulation increased the expression levels of GRP78, CHOP, NF‑κB and GrB, and decreased the expression of IκBα, and these changes were inhibited by SA3N, which indicated that inhibition of GrB activity may suppress endoplasmic reticulum (ER) stress signaling. Therefore, it was suggested that GrB may be a potential pro‑inflammatory factor, and inhibition of GrB activity may aid the prevention of the development of inflammation by suppressing ER stress signaling.
Starting Page	580
Ending Page	586
Page Count	7
File Format	PDF HTM / HTML
DOI	10.3892/mmr.2018.8995
PubMed reference number	29749522
Journal	Medline
Volume Number	18
Issue Number	1
Alternate Webpage(s)	https://www.spandidos-publications.com/mmr/18/1/580/download
Journal	Molecular medicine reports
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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