Unique roles of phosphorus in endochondral bone formation and osteocyte maturation.
Rong Zhang,Yongbo Lu,Ling Ye,Baozhi Yuan,Shibin Yu,Chunlin Qin,Yixia Xie,Tian Gao,Marc K. Drezner,Lynda F. Bonewald,Jian Q. Feng +10 more
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TLDR
It is shown that abnormal bone remodeling in Dmp1 null mice is due to reduced osteoclast number, which is secondary to a reduced ratio of RANKL/OPG expressed by osteoc Last supporting cells, and that osteoblast extracellular matrix mineralization, growth plate maturation, secondary ossification center formation, and osteOBlast differentiation are phosphate‐dependent.Abstract:
The mechanisms by which inorganic phosphate (Pi) homeostasis controls bone biology are poorly understood. Here we used Dmp1 null mice, a hypophosphatemic rickets/osteomalacia model, combined with a metatarsal organ culture and an application of neutralizing fibroblast growth factor 23 (FGF-23) antibodies to gain insight into the roles of Pi in bone biology. We showed (1) that abnormal bone remodeling in Dmp1 null mice is due to reduced osteoclast number, which is secondary to a reduced ratio of RANKL/OPG expressed by osteoclast supporting cells and (2) that osteoblast extracellular matrix mineralization, growth plate maturation, secondary ossification center formation, and osteoblast differentiation are phosphate-dependent. Finally, a working hypothesis is proposed to explain how phosphate and DMP1 control osteocyte maturation. © 2011 American Society for Bone and Mineral Research.read more
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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.
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Bioactive calcium phosphate materials and applications in bone regeneration
TL;DR: Calcium phosphate has been utilized to improve bone regeneration in ways such as increasing osteoconductivity for bone ingrowth, enhancing osteoinductivity in combination with various healing agents, and encapsulating drugs or growth factors.
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How smart do biomaterials need to be? A translational science and clinical point of view ☆
Boris Michael Holzapfel,Johannes C. Reichert,Jan-Thorsten Schantz,Uwe Gbureck,Lars Rackwitz,Ulrich Nöth,Franz Jakob,Maximilian Rudert,Jürgen Groll,Dietmar W. Hutmacher +9 more
TL;DR: The purpose of the review is to assess state of the art and future perspectives of the so called "smart biomaterials" from a translational science and specifically clinical point of view and to filter out and discuss which biomedical advances and innovations help to achieve the objective to translate smart biomMaterials from bench to bedside.
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Bioinorganics and biomaterials: bone repair.
TL;DR: It is illustrated that inorganics can positively affect bone healing but various factors make literature comparisons difficult and Bioinorganics have the potential to have just as big an impact on bone regeneration as recombinant proteins without some of the safety concerns and high costs.
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Transglutaminase Regulation of Cell Function
Richard L. Eckert,Mari T. Kaartinen,Maria Nurminskaya,Alexey M. Belkin,Gozde Colak,Gail V.W. Johnson,Kapil Mehta +6 more
TL;DR: The studies described herein begin to clarify the physiological roles of TGs in both normal biology and disease states and highlight the mechanism of action of these proteins with respect to their structure, impact on cell differentiation and survival, role in cancer development and progression.
References
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Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism
Takashi Shimada,Makoto Kakitani,Yuji Yamazaki,Hisashi Hasegawa,Yasuhiro Takeuchi,Toshiro Fujita,Seiji Fukumoto,Kazuma Tomizuka,Takeyoshi Yamashita +8 more
TL;DR: Evidence is presented that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF 23-null mice, indicating that F GF23 is essential for normal phosphate and vitamin D metabolism.
Journal ArticleDOI
Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia
Takashi Shimada,Satoru Mizutani,Takanori Muto,Takashi Yoneya,Rieko Hino,Shu Takeda,Yasuhiro Takeuchi,Toshiro Fujita,Seiji Fukumoto,Takeyoshi Yamashita +9 more
TL;DR: It is concluded that overproduction of F GF23 causes TIO, whereas mutations in the FGF23 gene result in autosomal dominant hypophosphatemic rickets possibly by preventing proteolytic cleavage and enhancing biological activity of FGF 23.
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.
Journal ArticleDOI
The parathyroid is a target organ for FGF23 in rats
Iddo Z. Ben-Dov,Hillel Galitzer,Vardit Lavi-Moshayoff,Regina Goetz,Makoto Kuro-o,Moosa Mohammadi,Roy Sirkis,Tally Naveh-Many,Justin Silver +8 more
TL;DR: It is shown that FGF23 acts directly on the parathyroid through the MAPK pathway to decrease serum PTH, which adds a new dimension to the understanding of mineral homeostasis.
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