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10.1038/nm.3654 http://scihub22266oqcxt.onion/10.1038/nm.3654 C4392888!4392888!25306233     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Med 2014 ; 20 (11): 1279-88 Nephropedia Template TP {{tp|p=25306233|t=2014. Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures |pdf=|usr=}}{{25306233}} gab.com Text Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures JO: Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=25306233 #FOAvip The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans. The disability, mortality and costs caused by osteoporosis-induced nonvertebral fractures are enormous. We demonstrate here that Wnt16-deficient mice develop spontaneous fractures as a result of low cortical thickness and high cortical porosity. In contrast, trabecular bone volume is not altered in these mice. Mechanistic studies revealed that WNT16 is osteoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast progenitors and indirectly by increasing expression of osteoprotegerin (Opg) in osteoblasts. The signaling pathway activated by WNT16 in osteoclast progenitors is noncanonical, whereas the pathway activated in osteoblasts is both canonical and noncanonical. Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT16, and its targeted deletion in osteoblasts increases fracture susceptibility. Thus, osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility. These findings open new avenues for the specific prevention or treatment of nonvertebral fractures, a substantial unmet medical need. Twit Text FOAVip Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures ????Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=25306233 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25306233 #FOAvip English Wikipedia <ref>{{Cite pmid|25306233}}</ref> Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures #MMPMID25306233 Movérare-Skrtic S; Henning P; Liu X; Nagano K; Saito H; Börjesson AE; Sjögren K; Windahl SH; Farman H; Kindlund B; Engdahl C; Koskela A; Zhang FP; Eriksson EE; Zaman F; Hammarstedt A; Isaksson H; Bally M; Kassem A; Lindholm C; Sandberg O; Aspenberg P; Sävendahl L; Feng JQ; Tuckermann J; Tuukkanen J; Poutanen M; Baron R; Lerner UH; Gori F; Ohlsson C Nat Med 2014[Nov]; 20 (11): 1279-88 PMID25306233show ga The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans. The disability, mortality and costs caused by osteoporosis-induced nonvertebral fractures are enormous. We demonstrate here that Wnt16-deficient mice develop spontaneous fractures as a result of low cortical thickness and high cortical porosity. In contrast, trabecular bone volume is not altered in these mice. Mechanistic studies revealed that WNT16 is osteoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast progenitors and indirectly by increasing expression of osteoprotegerin (Opg) in osteoblasts. The signaling pathway activated by WNT16 in osteoclast progenitors is noncanonical, whereas the pathway activated in osteoblasts is both canonical and noncanonical. Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT16, and its targeted deletion in osteoblasts increases fracture susceptibility. Thus, osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility. These findings open new avenues for the specific prevention or treatment of nonvertebral fractures, a substantial unmet medical need. äOsteoblast-derived WNT16 represses osteoclastogenesis and prevents cor(epmc).pdf DeepDyve Pubget Overpricing