Taurine Chloramine Inhibits Osteoclastic Differentiation and Osteoclast Marker Expression in RAW 264.7 Cells

Author(s):  
In Soon Kang ◽  
Chaekyun Kim
1993 ◽  
Vol 54 (2) ◽  
pp. 119-124 ◽  
Author(s):  
Eunkyue Park ◽  
Michael R. Quinn ◽  
Charles E. Wright ◽  
Georgia Schuller-Levis

2020 ◽  
Vol 20 (2) ◽  
pp. 152-161
Author(s):  
Hanwen Li ◽  
Yongyao Wu ◽  
Ning Huang ◽  
Qi Zhao ◽  
Quan Yuan ◽  
...  

Background: Osteoporosis is the most common metabolic bone disease. There is still an unmet need for novel therapeutic agents that could be beneficial as osteoporosis treatments. It has been reported that the neurotransmitter γ-aminobutyric acid (GABA) might be associated with human bone formation. However, the precise mechanism remains unclear. Objective: To investigate the effect of GABA on bone metabolism and explore the possible role of TNFAIP3 in this process. Methods: GABA had little effect on the proliferation of human mesenchymal stem cells (hMSCs) and RAW 264.7 cells, as indicated by the cell counting kit-8 (CCK-8) assay. The results showed that GABA enhanced the intensity of ALP staining, ALP activity, and accumulation of Ca2+ mineralized nodules in hMSCs during osteogenic induction. Results: The qRT-PCR results indicated that GABA treatment significantly increased the mRNA expression of osteogenic genes in hMSCs. In RAW 264.7 cells, TRAP staining showed that GABA did not alter the number or size of osteoclasts or the expression of osteoclastic genes, which suggests that GABA does not affect osteoclastic differentiation. Mechanistically, GABA treatment significantly induced the sustained expression of TNFAIP3. Furthermore, by knocking down TNFAIP3, the osteogenic effect of GABA was antagonized, which suggests that TNFAIP3 mediates the effects of GABA in hMSCs. Conclusion: Our results suggested that GABA treatment positively regulated osteogenic differentiation by upregulating TNFAIP3, while no obvious effect on osteoclastic differentiation was detected. Therefore, our results provide a potential gene therapy for the treatment of osteoporosis and low bone mineral density.


Nanomedicine ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. 1093-1105 ◽  
Author(s):  
Rainer Detsch ◽  
Matthias Rübner ◽  
Pamela L Strissel ◽  
Dirk Mohn ◽  
Erwin Strasser ◽  
...  

1997 ◽  
Vol 61 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Eunkyue Park ◽  
Georgia Schuller-Levis ◽  
Jun-Hua Jia ◽  
Michael R. Quinn

Author(s):  
Hnin Ei Thu ◽  
Zahid Hussain ◽  
Isa Naina Mohamed ◽  
Ahmad Nazrun Shuid

Objective: Numerous studies have evidenced the bone regulatory potential of dihydrotestosterone in androgen-deficient osteoporosis. The present study was thus aimed to explore the translational mechanism of dihydrotestosterone to down-regulate the bone resorption activity of osteoclasts using RAW 264.7 cells as in vitro model.Methods: Prior to analyze the efficacy of dihydrotestosterone (5α-DHT) to alleviate osteoclastic differentiation, their cell viability and cell proliferative ability was assessed using lactate dehydrogenase (LDH) and MTS assays. The osteoclastic differentiation capacity of dihydrotestosterone was evaluated by measuring TRAP activity and the expression of bone resorption-related proteins such as matrix metallopeptidase-9 (MMP-9), cathepsin-K, tartrate-resistant acid phosphatase (TRAP) and NFATc1. Moreover, the effects of dihydrotestosterone were also evaluated on superoxide (free radicals) generation and superoxide dismutase (SOD) activity in RANKL-induced osteoclasts.Results: Dihydrotestosterone showed no toxicity towards RAW 264.7 cells and significantly enhanced their proliferation and growth rates in a dose-dependent fashion. It was also observed that dihydrotestosterone exhibits a remarkable inhibitory effect on differentiation, maturation and activation of osteoclasts. The marked inhibition of differentiation and activation of osteoclasts caused by 5α-DHT was due to down-regulation of the expression of MMP-9, cathepsin-K, TRAP, NFATc1, generation of superoxide and up-regulation of SOD activity in the RAW 264.7 cells.Conclusion: Resulting data provided substantially in vitroevidence for the pronounced anti-osteoclastogenetic activity of dihydrotestosterone and its therapeutic value in treating osteoporosis and other bone-erosive disorders. 


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