understand the roles of SXR/PXR in the bone tissue more precisely. Our results demonstrated that loss of SXR/PXR enhanced bone resorption and reduced bone formation in the trabecular bones and decreased thickness in the cortical bones. Moreover, these mice
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Kotaro Azuma, Stephanie C Casey, Masako Ito, Tomohiko Urano, Kuniko Horie, Yasuyoshi Ouchi, Séverine Kirchner, Bruce Blumberg, and Satoshi Inoue
R Hardy and M S Cooper
bone remodelling cycle. Inflammatory disease can increase bone resorption, decrease bone formation but most commonly impacts on both of these processes. This review will illustrate these interactions between inflammation and bone metabolism and discuss
Chalida Nakalekha, Chieko Yokoyama, Hiroyuki Miura, Neil Alles, Kazuhiro Aoki, Keiichi Ohya, and Ikuo Morita
adult PGIS −/− mice, both bone formation and bone resorption parameters were increased ( Fig. 4 A–G). To determine whether the increase in trabecular bone mass was due to an acceleration in bone formation, a dynamic histomorphometric analysis was
Thomas Funck-Brentano, Karin H Nilsson, Robert Brommage, Petra Henning, Ulf H Lerner, Antti Koskela, Juha Tuukkanen, Martine Cohen-Solal, Sofia Movérare-Skrtic, and Claes Ohlsson
rate was unaffected ( P = 0.881; Fig. 3D ). The reduced periosteal bone formation and increased endocortical bone resorption were supported by the observation that Alpl mRNA levels ( P = 0.032) were reduced while Ctsk mRNA levels ( P < 0
Idris Mohamed and James K Yeh
resorption parameter were decreasing during this rapid-growth stage. L treatment resulted in a significant increase in the periosteal MAR, BFR/BS, endocortical MS/BS, MAR, BFR/BS, and the ErS/BS (%), while A had no significant effect on bone formation
J Jeyabalan, M Shah, B Viollet, J P Roux, P Chavassieux, M Korbonits, and C Chenu
). The relationship between AMPK activation and bone resorption is also unclear. Activation of AMPK was shown to inhibit osteoclast formation and bone resorption in vitro , AMPK acting as a negative regulator of RANKL ( Lee et al . 2010 ). By contrast
Russell T Turner, Kenneth A Philbrick, Carmen P Wong, Dawn A Olson, Adam J Branscum, and Urszula T Iwaniec
-deficient mice and leptin-receptor-deficient mice and rats have reduced overall bone mass, reduced longitudinal bone growth ( Steppan et al . 2000 , Kishida et al . 2005 ), and decreased bone formation ( Gat-Yablonski & Phillip 2008 ). In addition, impaired
Wang Xiao, Fei Beibei, Shen Guangsi, Jiang Yu, Zhang Wen, Huang Xi, and Xu Youjia
Significant difference with Con group ( P <0.05). Figure 2 Micro-CT three-dimensional reconstruction images and evaluation of oxidative stress, bone resorption, and bone formation markers in vivo . (A) Micro-CT images of mice belonging to the Con, F, OVX, and
Vikte Lionikaite, Karin L Gustafsson, Anna Westerlund, Sara H Windahl, Antti Koskela, Juha Tuukkanen, Helena Johansson, Claes Ohlsson, H Herschel Conaway, Petra Henning, and Ulf H Lerner
in long bones as well as in vertebra, paying special attention to osteoclastic bone resorption and osteoblastic bone formation. Materials and methods Animals and study design All animal experimental procedures were approved by the Ethics
Isabel R Orriss, Dilek Guneri, Mark O R Hajjawi, Kristy Shaw, Jessal J Patel, and Timothy R Arnett
until analysis. Levels of the bone formation marker, N-terminal propeptide of type I collagen (P1NP) and the bone resorption marker, cross-linked C-telopeptide (CTX), were assayed using the P1NP and RatLaps ELISAs, respectively (Immunodiagnostics Systems
