 |
 |
GEO help: Mouse over screen elements for information. |
|
| Status |
Public on Dec 30, 2018 |
| Title |
Dental pulp cell-derived powerful inducer of TNF-alpha comprises PKR containing stress granule rich microvesicles (GFvsDP-1) |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
|
| Summary |
It is well known that dental pulp tissue can evoke some of the most severe acute inflammation observed in the human body. We found that dental pulp cells secrete a factor that induces tumor necrosis factor-α production from macrophages, and designated this factor, dental pulp cell-derived tumor necrosis factor-α-inducing factor (DPTIF). DPTIF was induced in dental pulp cells and transported to recipient cells via microvesicles. Treatment of dental pulp cells with a PKR inhibitor markedly suppressed DPTIF activity, and weak interferon signals were constitutively activated inside the cells. In recipient macrophages, stimulation with DPTIF-containing supernatants from pulp cells resulted in activation of both nuclear factor-κB and MAP kinases like JNK and p38. Proteomics analyses revealed that many stress granule-related proteins were present in supernatants from dental pulp cells as well as microvesicle marker proteins like GAPDH, β-actin, HSPA8, HSPB1, HSPE1, and HSPD1. Furthermore, giant molecule AHNAK and PKR were detected in microvesicles derived from dental pulp cells, and gene silencing of AHNAK in pulp cells led to reduced DPTIF activity. Thus, it appeared that the core protein of DPTIF was PKR, and that PKR was maintained in an active state in stress granule aggregates with AHNAK and transported via microvesicles. The activity of DPTIF for TNF-α induction was far superior to that of gram-negative bacterial endotoxin. Therefore, we, report for the first time, that active PKR is transported via microvesicles as stress granule aggregates and induces powerful inflammatory signals in macrophages.
|
| |
|
| Overall design |
To determine the differences in gene expression between cells with and without dental pulp cell-derived tumor necrosis factor-α-inducing factor (DPTIF) activity, we compared gene expression profiles between immortalized dental pulp calls (DP-1) with DPTIF activity and gingival tissue-derived fibroblasts without DPTIF activity
|
| |
|
| Contributor(s) |
Suzuki S, Fukuda T, Nagayasu S, Nakanishi J, Yoshida K, Hirata-Tsuchiya S, Nakao Y, Sano T, Yamashita A, Yamada S, Shiba H, Ohta K, Nishimura F |
| Citation(s) |
30846715 |
| Submission date |
Dec 29, 2018 |
| Last update date |
Apr 01, 2019 |
| Contact name |
Takao Fukuda |
| Organization name |
Kyushu University
|
| Department |
Faculty of dental science
|
| Lab |
Division of oral rehabilitation
|
| Street address |
3-1-1 Maidashi, Higashi-ku,
|
| City |
Fukuoka |
| State/province |
Fukuoka |
| ZIP/Postal code |
812-8582 |
| Country |
Japan |
| |
|
| Platforms (1) |
| GPL14550 |
Agilent-028004 SurePrint G3 Human GE 8x60K Microarray (Probe Name Version) |
|
| Samples (2) |
|
| This SubSeries is part of SuperSeries: |
| GSE124492 |
Dental pulp cell-derived powerful inducer of TNF-alpha comprises PKR containing stress granule rich microvesicles |
|
| Relations |
| BioProject |
PRJNA512200 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE124490_RAW.tar |
24.2 Mb |
(http)(custom) |
TAR (of TXT) |
| Processed data included within Sample table |
|
|
|
|
 |
