Ginsenoside Rb2 inhibits osteoclast differentiation through nuclear factor-kappaB and signal transducer and activator of transcription protein 3 signaling pathway

2017 ◽  
Vol 92 ◽  
pp. 927-934 ◽  
Author(s):  
Fei Cong ◽  
Jian Liu ◽  
Chunmei Wang ◽  
Zhi Yuan ◽  
Long Bi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Osteoclast Differentiation ◽  
Nuclear Factor Kappab ◽  
Nuclear Factor ◽  
Signal Transducer ◽  
Ginsenoside Rb2

Regulation of Nuclear Factor-KappaB (NF-κB) signaling pathway by non-coding RNAs in cancer: Inhibiting or promoting carcinogenesis?

2021 ◽  
Vol 509 ◽  
pp. 63-80 ◽  
Author(s):  
Sepideh Mirzaei ◽  
Ali Zarrabi ◽  
Farid Hashemi ◽  
Amirhossein Zabolian ◽  
Hossein Saleki ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nuclear Factor Kappab ◽  
Nuclear Factor ◽  
Non Coding Rnas

scholarly journals Interleukin-6 Inhibits Receptor Activator of Nuclear Factor κB Ligand-Induced Osteoclastogenesis by Diverting Cells into the Macrophage Lineage: Key Role of Serine727 Phosphorylation of Signal Transducer and Activator of Transcription 3

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3688-3697 ◽  
Author(s):  
Laurence Duplomb ◽  
Marc Baud’huin ◽  
Céline Charrier ◽  
Martine Berreur ◽  
Valérie Trichet ◽  
...  
Keyword(s):  
Osteoclast Differentiation ◽  
Nuclear Factor Κb ◽  
Mouse Bone Marrow ◽  
Nuclear Factor ◽  
Signal Transducer ◽  
Blood Monocytes ◽  
Receptor Activator ◽  
Few Data ◽  
Macrophage Lineage

Osteoclasts are bone-resorptive cells that differentiate from hematopoietic precursors upon receptor activator of nuclear factor κB ligand (RANKL) activation. Previous studies demonstrated that IL-6 indirectly stimulates osteoclastogenesis through the production of RANKL by osteoblasts. However, few data described the direct effect of IL-6 on osteoclasts. To investigate this effect, we used several models: murine RAW264.7 cells, mouse bone marrow, and human blood monocytes. In the three models used, the addition of IL-6 inhibited RANKL-induced osteoclastogenesis. Furthermore, IL-6 decreased the expression of osteoclast markers and up-modulated macrophage markers. To elucidate this inhibition, signal transducer and activator of transcription (STAT) 3, the main signaling molecule activated by IL-6, was analyzed. Addition of two STAT3 inhibitors completely abolished RANKL-induced osteoclastogenesis, revealing a key role of STAT3. We demonstrated that a basal level of phosphorylated-STAT3 on Serine727 associated with an absence of phosphorylation on Tyrosine705 is essential for osteoclastogenesis. Furthermore, a decrease of Serine727 phosphorylation led to an inhibition of osteoclast differentiation, whereas an increase of Tyrosine705 phosphorylation upon IL-6 stimulation led to the formation of macrophages instead of osteoclasts. In conclusion, we showed for the first time that IL-6 inhibits RANKL-induced osteoclastogenesis by diverting cells into the macrophage lineage, and demonstrated the functional role of activated-STAT3 and its form of phosphorylation in the control of osteoclastogenesis.

Activation of nuclear factor-kappaB signaling pathway by interleukin-1 after hypoxia/ischemia in neonatal rat hippocampus and cortex

2005 ◽  
Vol 93 (1) ◽  
pp. 26-37 ◽  
Author(s):  
Xiaoming Hu ◽  
Olivera Nesic-Taylor ◽  
Jingxin Qiu ◽  
Harriett C. Rea ◽  
Roderick Fabian ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Interleukin 1 ◽  
Rat Hippocampus ◽  
Neonatal Rat ◽  
Nuclear Factor Kappab ◽  
Nuclear Factor ◽  
Hypoxia Ischemia
Sign in / Sign up

Export Citation Format

Share Document