Henry M. Goldman School of Dental Medicine, Department of Periodontology, Boston University, 650 Albany Street, Boston, MA, USA.
Hum Cell. 2021 Jul;34(4):1123-1129. doi: 10.1007/s13577-021-00529-9. Epub 2021 Apr 28.
It is known that Porphyromonas gingivalis/lipopolysaccharide (P. gingivalis/LPS) induces inflammatory diseases via TNF-α-mediated transcription factors. Our recent data shows that TNFAIP1 (TNF-α induced protein 1) is related to TNF-α. However, little is known regarding how TNFAIP1 is involved in the TNF-α-dependent pathway. We therefore focused on the biological function of TNFAIP1 and examined how TNFAIP1 mediates TNF-α and other genes. We found that TNF-α was upregulated and peaks before the upregulation of apoptotic genes such as Bad, Bcl-x, Caspase 3, Catalase, Claspin, Cytochromic, Ho-1/HMOX1/HSP32, or MCI-1 in our time course with TNFAIP1-treated cells. Our findings here may serve as the foundation for future studies linking regulation of TNFAIP1 and intervention of inflammatory disease.
已知牙龈卟啉单胞菌/脂多糖（P. gingivalis/LPS）通过 TNF-α 介导的转录因子诱导炎症性疾病。我们最近的数据表明，TNFAIP1（TNF-α 诱导蛋白 1）与 TNF-α 有关。然而，关于 TNFAIP1 如何参与 TNF-α 依赖性途径知之甚少。因此，我们专注于 TNFAIP1 的生物学功能，并研究了 TNFAIP1 如何介导 TNF-α 和其他基因。我们发现，在 TNFAIP1 处理的细胞的时程中，TNF-α 的上调先于凋亡基因（如 Bad、Bcl-x、Caspase 3、Catalase、Claspin、Cytochromic、Ho-1/HMOX1/HSP32 或 MCI-1）的上调。我们在这里的发现可能为未来研究 TNFAIP1 的调节和炎症性疾病的干预提供基础。
