Доступ предоставлен для: Guest
Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Eukaryotic Gene Expression
Импакт фактор: 1.841 5-летний Импакт фактор: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN Печать: 1045-4403
ISSN Онлайн: 2162-6502

Выпуски:
Том 29, 2019 Том 28, 2018 Том 27, 2017 Том 26, 2016 Том 25, 2015 Том 24, 2014 Том 23, 2013 Том 22, 2012 Том 21, 2011 Том 20, 2010 Том 19, 2009 Том 18, 2008 Том 17, 2007 Том 16, 2006 Том 15, 2005 Том 14, 2004 Том 13, 2003 Том 12, 2002 Том 11, 2001 Том 10, 2000 Том 9, 1999 Том 8, 1998 Том 7, 1997 Том 6, 1996 Том 5, 1995 Том 4, 1994

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v19.i1.30
pages 61-72

Action of RANKL and OPG for Osteoclastogenesis

Yasuhiro Kobayashi
Division of Hard Tissue Research, Institute for Oral Science, Matsumoto Dental University, Shiojiri 399-0781, Japan
Nobuyuki Udagawa
Division of Hard Tissue Research, Institute for Oral Science, Matsumoto Dental University, Shiojiri 399-0781, Japan
Naoyuki Takahashi
Division of Hard Tissue Research, Institute for Oral Science, Matsumoto Dental University, Shiojiri 399-0781, Japan

Краткое описание

Osteoclasts develop from hematopoietic cells of the monocyte-macrophage lineage. The coculture system of osteoblasts and hematopoietic cells was devised to examine osteoclastogenesis in vitro. Experiments using the coculture system have established the concept that osteoblasts are crucially involved in osteoclastogenesis. Remarkable progress has been achieved during the last decade in our understanding the molecular mechanism of osteoclast differentiation, largely because of the discovery of receptor activator of NF-κB ligand (RANKL), an essential cytokine for osteoclastogenesis. Osteoblasts express RANKL in response to bone-resorbing factors. Osteoblasts also produce osteoprotegerin (OPG), a decoy receptor for RANKL, which inhibits osteoclast differentiation and function by interrupting the interaction between RANKL and RANK, a receptor of RANKL. The identification of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) as a master transcription factor for RANKL-induced osteoclastogenesis has provided major insight into the molecular mechanism of osteoclast differentiation. The discovery of the immunoreceptor tyrosine-based activation motif (ITAM)-mediated signals as a costimulatory signal in osteoclastogenesis has confirmed that osteoblasts play another important role in osteoclastogenesis. Mutations of RANK, OPG, and RANKL found in humans cause bone diseases associated with expected skeletal abnormalities. Thus, the RANKL/RANK/OPG axis is now recognized as the central regulator of osteoclast differentiation and function.


Articles with similar content:

Regulatory Mechanisms Operative in Osteoclasts
Critical Reviews™ in Eukaryotic Gene Expression, Vol.14, 2004, issue 4
Sakamuri V. Reddy
Interleukins in the Control of Osteoclast Differentiation
Critical Reviews™ in Eukaryotic Gene Expression, Vol.8, 1998, issue 2
M. T. Gillespie, E. Romas, T. John Martin
lnterleukin-16: The Ins and Outs of Regulating T-Cell Activation
Critical Reviews™ in Immunology, Vol.28, 2008, issue 6
Frederic Little, William Cruikshank
Does TNF Promote or Restrain Osteoclastogenesis and Inflammatory Bone Resorption?
Critical Reviews™ in Immunology, Vol.38, 2018, issue 4
Baohong Zhao
The Ron Receptor Tyrosine Kinase: A Key Regulator of Inflammation and Cancer Progression
Critical Reviews™ in Immunology, Vol.33, 2013, issue 6
Pamela A. Hankey, Xin Wang