Demonstration of osteocytic perilacunar/canalicular remodeling in mice during lactation
Hai Qing,Laleh Ardeshirpour,Paola Divieti Pajevic,Vladimir Dusevich,Katharina Jähn,Shigeaki Kato,John J. Wysolmerski,Lynda F. Bonewald +7 more
TLDR
It is shown that osteocytes can also remove bone matrix by reversibly remodeling their perilacunar/canalicular matrix during the reproductive cycle through molecular mechanisms similar to those utilized by osteoclasts.Abstract:
Osteoclasts are thought to be solely responsible for the removal of bone matrix. However, we show here that osteocytes can also remove bone matrix by reversibly remodeling their perilacunar/canalicular matrix during the reproductive cycle. In contrast, no osteocytic remodeling was observed with experimental unloading despite similar degrees of bone loss. Gene array analysis of osteocytes from lactating animals revealed an elevation of genes known to be utilized by osteoclasts to remove bone, including tartrate-resistant acid phosphatase (TRAP) and cathepsin K, that returned to virgin levels upon weaning. Infusion of parathyroid hormone-related peptide (PTHrP), known to be elevated during lactation, induced TRAP activity and cathepsin K expression in osteocytes concurrent with osteocytic remodeling. Conversely, animals lacking the parathyroid hormone type 1 receptor (PTHR1) in osteocytes failed to express TRAP or cathepsin K or to remodel their osteocyte perilacunar matrix during lactation. These studies show that osteocytes remove mineralized matrix through molecular mechanisms similar to those utilized by osteoclasts.read more
Citations
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The Osteocyte: An Endocrine Cell … and More
TL;DR: The osteocytes encased within mineralized bone matrix are actually multifunctional cells with many key regulatory roles in bone and mineral homeostasis and should be considered in new strategies to prevent and treat bone disease.
Journal ArticleDOI
Targeting cellular senescence prevents age-related bone loss in mice
Joshua N. Farr,Ming Xu,Megan M. Weivoda,David G. Monroe,Daniel G. Fraser,Jennifer L Onken,Brittany A Negley,Jad G Sfeir,Mikolaj Ogrodnik,Christine M Hachfeld,Nathan K. LeBrasseur,Matthew T. Drake,Robert J. Pignolo,Tamar Pirtskhalava,Tamara Tchkonia,Merry Jo Oursler,James L. Kirkland,Sundeep Khosla +17 more
TL;DR: A causal role for senescent cells in bone loss with aging is established, and targeting these cells has both anti-resorptive and anabolic effects on bone, which suggests a novel treatment strategy not only for osteoporosis, but also for multiple age-related comorbidities.
Journal ArticleDOI
Osteocytes: Master Orchestrators of Bone
TL;DR: How a highly productive combination of experimental and theoretical approaches has managed to unearth unique features of osteocytes and bring to light novel insights into the regulatory mechanisms operating in bone is discussed.
Journal ArticleDOI
Irisin Mediates Effects on Bone and Fat via αV Integrin Receptors
Hyeonwoo Kim,Christiane D. Wrann,Mark P. Jedrychowski,Sara Vidoni,Yukiko Kitase,Kenichi Nagano,Chuan Zhou,Joshua Chou,Virginia-Jeni A. Parkman,Scott J. Novick,Timothy S. Strutzenberg,Bruce D. Pascal,Phuong T. Le,Daniel J. Brooks,Alexander M. Roche,Kaitlyn K. Gerber,Laura Mattheis,Wei Chen,Hua Tu,Mary L. Bouxsein,Patrick R. Griffin,Roland Baron,Clifford J. Rosen,Lynda F. Bonewald,Bruce M. Spiegelman +24 more
TL;DR: Irisin is secreted by muscle, increases with exercise, and mediates certain favorable effects of physical activity as discussed by the authors, however, the skeletal response to exercise is less clear, and the receptor for irisin has not been identified.
Journal ArticleDOI
Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery
TL;DR: This review addresses the current knowledge regarding maternal adaptations in mineral and skeletal homeostasis that occur during pregnancy, lactation, and post-weaning recovery and the impacts that these adaptations have on biochemical and hormonal parameters of mineralHomeostasis.
References
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Journal ArticleDOI
The Amazing Osteocyte
TL;DR: Osteocytes compose 90% to 95% of all bone cells in adult bone and are the longest lived bone cell, up to decades within their mineralized environment.
Journal ArticleDOI
Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism
Jian Q. Feng,Leanne M Ward,Shiguang Liu,Yongbo Lu,Yixia Xie,Baozhi Yuan,Xijie Yu,Frank Rauch,Siobhan I. Davis,Shubin Zhang,Hector F. Rios,Marc K. Drezner,L. Darryl Quarles,Lynda F. Bonewald,Kenneth E. White +14 more
TL;DR: Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization, suggesting a bone-renal axis that is central to guiding proper mineral metabolism.
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Sclerostin is a delayed secreted product of osteocytes that inhibits bone formation
Kenneth E. S. Poole,Rutger L. van Bezooijen,Nigel Loveridge,Herman Hamersma,Socrates E. Papapoulos,Clemens W.G.M. Löwik,Jonathan Reeve +6 more
TL;DR: In vivo evidence is provided for the first time to support the concept that osteocytes secrete sclerostin after they become embedded in a mineralized matrix to limit further bone formation by osteoblasts and propose that sclerOSTin production by osteocytes may regulate the linear extent of formation and the induction or maintenance of a lining cell phenotype on bone surfaces.
Journal ArticleDOI
Estrogen Prevents Bone Loss via Estrogen Receptor α and Induction of Fas Ligand in Osteoclasts
Takashi Nakamura,Yuuki Imai,Yuuki Imai,Takahiro Matsumoto,Shingo Sato,Kazusane Takeuchi,Katsuhide Igarashi,Yoshifumi Harada,Yoshiaki Azuma,Andrée Krust,Yoko Yamamoto,Hiroshi Nishina,Shu Takeda,Hiroshi Takayanagi,Daniel Metzger,Jun Kanno,Kunio Takaoka,T. John Martin,Pierre Chambon,Shigeaki Kato +19 more
TL;DR: A model in which estrogen regulates the life span of mature osteoclasts via the induction of the Fas/FasL system is supported, thereby providing an explanation for the osteoprotective function of estrogen as well as SERMs.