دورية أكاديمية
أعرض في EDS

Selenoprotein W engages in overactive osteoclast differentiation in multiple myeloma.

التفاصيل البيبلوغرافية
العنوان: Selenoprotein W engages in overactive osteoclast differentiation in multiple myeloma.
المؤلفون: Kim H; Laboratory of Bone Metabolism and Control, Department of Microbiology, Yeungnam University College of Medicine, Daegu, 42415, Korea.; Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA19104, USA., Oh J; Laboratory of Bone Metabolism and Control, Department of Microbiology, Yeungnam University College of Medicine, Daegu, 42415, Korea., Kim MK; Department of Hematology-Oncology, Yeungnam University College of Medicine, Daegu, 42415, Korea., Lee KH; Department of Hematology-Oncology, Yeungnam University College of Medicine, Daegu, 42415, Korea., Jeong D; Laboratory of Bone Metabolism and Control, Department of Microbiology, Yeungnam University College of Medicine, Daegu, 42415, Korea. dwjeong@ynu.ac.kr.; Company of The Bone Science, Yeungnam University College of Medicine, Daegu, 42415, Korea. dwjeong@ynu.ac.kr.
المصدر: Molecular biology reports [Mol Biol Rep] 2024 Apr 29; Vol. 51 (1), pp. 587. Date of Electronic Publication: 2024 Apr 29.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Reidel Country of Publication: Netherlands NLM ID: 0403234 Publication Model: Electronic Cited Medium: Internet ISSN: 1573-4978 (Electronic) Linking ISSN: 03014851 NLM ISO Abbreviation: Mol Biol Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Dordrecht, Boston, Reidel.
مواضيع طبية MeSH: Cell Differentiation*/genetics , Multiple Myeloma*/metabolism , Multiple Myeloma*/pathology , Multiple Myeloma*/genetics , Osteoclasts*/metabolism , Selenoprotein W*/metabolism , Selenoprotein W*/genetics, Animals ; Female ; Humans ; Male ; Mice ; Middle Aged ; Leukocytes, Mononuclear/metabolism ; MAP Kinase Signaling System ; NF-kappa B/metabolism ; NFATC Transcription Factors/metabolism ; NFATC Transcription Factors/genetics ; RANK Ligand/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism
مستخلص: Background: Patients with multiple myeloma exhibit malignant osteolytic bone disease due to excessive osteoclast formation and function. We recently identified that osteoclastogenic stimulator selenoprotein W (SELENOW) is upregulated via ERK signaling and downregulated via p38 signaling during receptor activator of nuclear factor (NF)-κΒ ligand (RANKL)-induced osteoclast differentiation. In the intrinsic physiological process, RANKL-induced downregulation of SELENOW maintains proper osteoclast differentiation; in contrast, forced overexpression of SELENOW leads to overactive osteoclast formation and function.
Methods and Results: We observed that SELENOW is highly expressed in multiple myeloma-derived peripheral blood mononuclear cells (PBMCs) and mature osteoclasts when compared to healthy controls. Also, the level of tumor necrosis factor alpha (TNFα), a pathological osteoclastogenic factor, is increased in the PBMCs and serum of patients with multiple myeloma. ERK activation by TNFα was more marked and sustained than that by RANKL, allowing SELENOW upregulation. Excessive expression of SELENOW in osteoclast progenitors and mature osteoclasts derived from multiple myeloma facilitated efficient nuclear translocation of osteoclastogenic transcription factors NF-κB and NFATc1, which are favorable for osteoclast formation.
Conclusion: Our findings suggest a possibility that feedforward signaling of osteoclastogenic SELENOW by TNFα derived from multiple myeloma induces overactive osteoclast differentiation, leading to bone loss during multiple myeloma.
(© 2024. The Author(s).)
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معلومات مُعتمدة: 2022R1A2C1002736 and 2022R1A5A2018865 National Research Foundation of Korea
فهرسة مساهمة: Keywords: Bone disease; Multiple myeloma; Osteoclast differentiation; Selenoprotein W
المشرفين على المادة: 0 (NF-kappa B)
0 (NFATC Transcription Factors)
0 (NFATC1 protein, human)
0 (RANK Ligand)
0 (Selenoprotein W)
0 (TNFSF11 protein, human)
0 (Tumor Necrosis Factor-alpha)
0 (SELENOW protein, human)
تواريخ الأحداث: Date Created: 20240429 Date Completed: 20240429 Latest Revision: 20240509
رمز التحديث: 20240509
مُعرف محوري في PubMed: PMC11058866
DOI: 10.1007/s11033-024-09517-2
PMID: 38683225
قاعدة البيانات: MEDLINE
الوصف
تدمد:1573-4978
DOI:10.1007/s11033-024-09517-2