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Abstract Number: 1962

The Specific Role of Glutaredoxin2 Isoform b (Glrx2b) in RANKL-Induced Osteoclastogenesis Through Activation of the p38-MAPK Signaling Pathway

Chang-Hoon Lee1, Wan-Hee Yoo2, Jin-Jung Choi3, Myong-Joo Hong4, Ji-Min Kim5 and Jeong-Tae Yeon6, 1Department of Internal Medicine, School of medicine, Wonkwang university, Iksan, Chonbuk, South Korea, 2Department of Internal Medicine, Chonbuk National University Medical School and Research Institute of Clinical Medicine, Jeonju, South Korea, 3Internal Medicine, CHA University Hospital, Seongnam, South Korea, 4Rheumatology, Department of Internal Medicine, Chonbuk National University Medical School and Research Institute of Clinical Medicine, Jeonju, South Korea, 5Division of Rheumatology, Department of Internal Medicine, Keimyung University School of Medicine, Daegu, South Korea, 6Department of anatomy, school of medicine, Wonkwang university, Iksan, Chonbuk, South Korea

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: antioxidants and osteoclastogenesis, RANK/RANKL pathway

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Session Information

Title: Osteoporosis and Metabolic Bone Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: Recently, reactive oxygen species (ROS) and antioxidant enzymes were shown to be closely associated with RANKL-mediated osteoclast differentiation. Although glutaredoxin2 (Glrx2) plays a role in cellular redox homeostasis, its role in RANKL-mediated osteoclastogenesis is unclear.

Objectives : The aim of this study was to examine the effect of Glrx2 on osteoclast differentiation

Methods: Osteoclast formation was evaluated in bone marrow cells (BMC) in specific condition with over-expression of Glrx2 or down- regulation of Glrx2 during receptor activator of NF-κB ligand (RANKL)- mediated  osteoclastogenesis.. The expression of c-fos and NFATc1 mRNA in osteoclast precursor were assessed by RT-PCR. The levels of c-fos and NFATc1 protein were assessed by western blot. Also the mitogen-activated protein (MAPK)s pathways were measured using Western blot analysis

Results: We found that Glrx2 isoform b (Glrx2b) expression is induced during RANKL-mediated osteoclastogenesis. Over-expression of Glrx2b strongly enhanced RANKL-mediated osteoclastogenesis. In addition, Glrx2b-transduced BMMs enhanced the expression of key transcription factors c-Fos and NFATc1, but pre-treatment with SB203580, a p38-specific inhibitor, completely blocked this enhancement. Conversely, down-regulation of Glrx2b decreased RANKL-mediated osteoclastogenesis and the expression of c-Fos and NFATc1 proteins. Also, Glrx2b down-regulation attenuated the RANKL-induced activation of p38.

 Conclusion: Taken together, these results suggest that Glrx2b enhances RANKL-induced osteoclastogenesis via p38 activation. It may be very useful information for treatment of bone-resorbing disorders, such as rheumatoid arthritis and osteoporosis.


Disclosure:

C. H. Lee,
None;

W. H. Yoo,
None;

J. J. Choi,
None;

M. J. Hong,
None;

J. M. Kim,
None;

J. T. Yeon,
None.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/the-specific-role-of-glutaredoxin2-isoform-b-glrx2b-in-rankl-induced-osteoclastogenesis-through-activation-of-the-p38-mapk-signaling-pathway/

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