MicroRNA-26a Regulates RANKL-Induced Osteoclast Formation

Kim, Kabsun; Kim, Jung Ha; Kim, In-Young; Lee, Jongwon; Seong, Semun; Park, Yong-Wook; Kim, Nacksung

doi:10.14348/molcells.2015.2241

Cited by 68 publications

(29 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Murine osteoclasts were prepared from bone marrow cells as previously described ( Kim et al, 2007 ; 2015 ). In brief, mouse bone marrow cells were isolated from tibiae and femurs of 6–8 week old ICR mice by flushing the bone marrows with α-minimal essential medium (α-MEM).…”

Section: Methodsmentioning

confidence: 99%

NRROS Negatively Regulates Osteoclast Differentiation by Inhibiting RANKL-Mediated NF-κB and Reactive Oxygen Species Pathways

Kim

et al. 2015

Molecules and Cells

View full text Add to dashboard Cite

Negative regulator of reactive oxygen species (NRROS) is known to repress ROS generation in phagocytes. In this study, we examined the roles of NRROS in both osteoclasts and osteoblasts. Our results demonstrate that NRROS negatively regulates the differentiation of osteoclasts, but not osteoblasts. Further, overexpression of NRROS in osteoclast precursor cells attenuates RANKL-induced osteoclast differentiation. Conversely, osteoclast differentiation is enhanced upon siRNA-mediated knockdown of NRROS. Additionally, NRROS attenuates RANKL-induced NF-κB activation, as well as degradation of the NOX1 and NOX2 proteins, which are required for ROS generation. Based on our observations, we present NRROS as a novel negative regulator of RANKL-induced osteoclastogenesis.

show abstract

Section: Methodsmentioning

confidence: 99%

NRROS Negatively Regulates Osteoclast Differentiation by Inhibiting RANKL-Mediated NF-κB and Reactive Oxygen Species Pathways

Kim

et al. 2015

Molecules and Cells

View full text Add to dashboard Cite

show abstract

“…Data suggest that this may be through epigenetic regulation [ 4 , 7 , 81 , 82 , 83 , 84 , 85 , 86 ]. An epigenetic regulation of the DCSTAMP gene is interesting, because it may be a tool to regulate this powerful regulator of osteoclast multinucleation both through DNA methylation [ 7 , 81 ], histone methylation [ 86 ], and miRNA [ 82 , 83 , 84 , 85 ]. Studies of Møller et al [ 4 , 7 ] have shown that DNA methylation levels of the DCSTAMP gene are lower with increasing age and that this results in an elevated gene expression, multinucleation, and bone resorptive activity of osteoclasts in vitro.…”

Section: Regulation Of Multinucleationmentioning

confidence: 99%

Osteoclast Fusion: Physiological Regulation of Multinucleation through Heterogeneity—Potential Implications for Drug Sensitivity

Søe

2020

IJMS

View full text Add to dashboard Cite

Classically, osteoclast fusion consists of four basic steps: (1) attraction/migration, (2) recognition, (3) cell–cell adhesion, and (4) membrane fusion. In theory, this sounds like a straightforward simple linear process. However, it is not. Osteoclast fusion has to take place in a well-coordinated manner—something that is not simple. In vivo, the complex regulation of osteoclast formation takes place within the bone marrow—in time and space. The present review will focus on considering osteoclast fusion in the context of physiology and pathology. Special attention is given to: (1) regulation of osteoclast fusion in vivo, (2) heterogeneity of osteoclast fusion partners, (3) regulation of multi-nucleation, (4) implications for physiology and pathology, and (5) implications for drug sensitivity and side effects. The review will emphasize that more attention should be given to the human in vivo reality when interpreting the impact of in vitro and animal studies. This should be done in order to improve our understanding of human physiology and pathology, as well as to improve anti-resorptive treatment and reduce side effects.

show abstract

“… 184 In addition, connective tissue growth factor (CTGF) has the dual ability of promoting endochondral ossification and increasing RANKL-mediated osteoclastogenesis. 185 , 186 …”

Section: Mirnas In Osteoclast Lineage and Bone Resorptionmentioning

confidence: 99%

The role of microRNAs in bone remodeling

et al. 2015

View full text Add to dashboard Cite

Bone remodeling is balanced by bone formation and bone resorption as well as by alterations in the quantities and functions of seed cells, leading to either the maintenance or deterioration of bone status. The existing evidence indicates that microRNAs (miRNAs), known as a family of short non-coding RNAs, are the key post-transcriptional repressors of gene expression, and growing numbers of novel miRNAs have been verified to play vital roles in the regulation of osteogenesis, osteoclastogenesis, and adipogenesis, revealing how they interact with signaling molecules to control these processes. This review summarizes the current knowledge of the roles of miRNAs in regulating bone remodeling as well as novel applications for miRNAs in biomaterials for therapeutic purposes.

show abstract

MicroRNA-26a Regulates RANKL-Induced Osteoclast Formation

Cited by 68 publications

References 26 publications

NRROS Negatively Regulates Osteoclast Differentiation by Inhibiting RANKL-Mediated NF-κB and Reactive Oxygen Species Pathways

NRROS Negatively Regulates Osteoclast Differentiation by Inhibiting RANKL-Mediated NF-κB and Reactive Oxygen Species Pathways

Osteoclast Fusion: Physiological Regulation of Multinucleation through Heterogeneity—Potential Implications for Drug Sensitivity

The role of microRNAs in bone remodeling

Contact Info

Product

Resources

About