Interleukin-6 transiently promotes proliferation of osteoclast precursors and stimulates the production of inflammatory mediators.
Peng-Yuan ChangHung-Kang WuYu-Hsu ChenYu-Pao HsuMing-Te ChengChing-Hsiao YuShau-Kwaun ChenPublished in: Molecular biology reports (2022)
IL-6 triggered transient proliferation, but not apoptosis, in RANKL-stimulated RAW cells. Osteoclastogenesis was disrupted as the expression of essential genes for bone resorption were inhibited, and the osteoclast precursors maintained their undifferentiated phenotypes, with pro-inflammatory genes upregulated. Our results suggested that IL-6 interferes osteoclastogenesis. Additionally, IL-6 promote pro-inflammatory responses of monocytic cells and aggravate inflammation.
Keyphrases
- bone loss
- cell cycle arrest
- induced apoptosis
- oxidative stress
- signaling pathway
- endoplasmic reticulum stress
- cell death
- pi k akt
- genome wide
- poor prognosis
- gene expression
- bioinformatics analysis
- resting state
- toll like receptor
- brain injury
- subarachnoid hemorrhage
- body composition
- anti inflammatory
- functional connectivity
- binding protein
- genome wide analysis
- cerebral ischemia