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Title: The Local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth.
Authors: Nakao, Kazumasa
Osawa, Kenji
Yasoda, Akihiro  kyouindb  KAKEN_id
Yamanaka, Shigeki
Fujii, Toshihito  kyouindb  KAKEN_id
Kondo, Eri
Koyama, Noriaki
Kanamoto, Naotetsu
Miura, Masako
Kuwahara, Koichiro  KAKEN_id
Akiyama, Haruhiko
Bessho, Kazuhisa  kyouindb  KAKEN_id
Nakao, Kazuwa
Author's alias: 八十田, 明宏
Issue Date: 27-May-2015
Publisher: Nature Publishing Group
Journal title: Scientific reports
Volume: 5
Thesis number: 10554
Abstract: Recent studies revealed C-type natriuretic peptide (CNP) and its receptor, guanylyl cyclase-B (GC-B) are potent stimulators of endochondral bone growth. As they exist ubiquitously in body, we investigated the physiological role of the local CNP/GC-B in the growth plate on bone growth using cartilage-specific knockout mice. Bones were severely shorter in cartilage-specific CNP or GC-B knockout mice and the extent was almost the same as that in respective systemic knockout mice. Cartilage-specific GC-B knockout mice were shorter than cartilage-specific CNP knockout mice. Hypertrophic chondrocyte layer of the growth plate was drastically reduced and proliferative chondrocyte layer, along with the proliferation of chondrocytes there, was moderately reduced in either cartilage-specific knockout mice. The survival rate of cartilage-specific CNP knockout mice was comparable to that of systemic CNP knockout mice. The local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth and might further affect mortality via unknown mechanisms.
Rights: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
DOI(Published Version): 10.1038/srep10554
PubMed ID: 26014585
Appears in Collections:Journal Articles

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