Institution
Research Triangle Park
Nonprofit•Durham, North Carolina, United States•
About: Research Triangle Park is a nonprofit organization based out in Durham, North Carolina, United States. It is known for research contribution in the topics: Population & Receptor. The organization has 24961 authors who have published 35800 publications receiving 1684504 citations. The organization is also known as: RTP.
Topics: Population, Receptor, Health care, Gene, Environmental exposure
Papers published on a yearly basis
Papers
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262 citations
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TL;DR: The consensus of the group was that the maximum birth spacing effect of breastfeeding is achieved when a mother "fully" or nearly fully breastfeeds and remains amenorrheic.
262 citations
01 Sep 2008
262 citations
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TL;DR: A distinct alteration in the slope of the survival curve after 6 months of lamivudine treatment for decompensated chronic hepatitis B is demonstrated, which may help identify patients who can be stabilized with suppressive antiviral therapy vs. those who require urgent liver transplantation.
262 citations
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TL;DR: It is demonstrated that BMPR1A signaling in osteoblasts restrain endogenous bone mass directly by upregulating osteoclastogenesis through the RANKL-OPG pathway, or indirectly by downregulating canonical Wnt signaling through sclerostin, a Wnt inhibitor and a bone mass mediator.
Abstract: Bone morphogenetic proteins (BMPs) are known to induce ectopic bone. However, it is largely unknown how BMP signaling in osteoblasts directly regulates endogenous bone. This study investigated the mechanism by which BMP signaling through the type IA receptor (BMPR1A) regulates endogenous bone mass using an inducible Cre-loxP system. When BMPR1A in osteoblasts was conditionally disrupted during embryonic bone development, bone mass surprisingly was increased with upregulation of canonical Wnt signaling. Although levels of bone formation markers were modestly reduced, levels of resorption markers representing osteoclastogenesis were severely reduced, resulting in a net increase in bone mass. The reduction of osteoclastogenesis was primarily caused by Bmpr1a-deficiency in osteoblasts, at least through the RANKL-OPG pathway. Sclerostin (Sost) expression was downregulated by about 90% and SOST protein was undetectable in osteoblasts and osteocytes, whereas the Wnt signaling was upregulated. Treatment of Bmpr1a-deficient calvariae with sclerostin repressed the Wnt signaling and restored normal bone morphology. By gain of Smad-dependent BMPR1A signaling in mice, Sost expression was upregulated and osteoclastogenesis was increased. Finally, the Bmpr1a-deficient bone phenotype was rescued by enhancing BMPR1A signaling, with restoration of osteoclastogenesis. These findings demonstrate that BMPR1A signaling in osteoblasts restrain endogenous bone mass directly by upregulating osteoclastogenesis through the RANKL-OPG pathway, or indirectly by downregulating canonical Wnt signaling through sclerostin, a Wnt inhibitor and a bone mass mediator.
262 citations
Authors
Showing all 25006 results
Name | H-index | Papers | Citations |
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Douglas G. Altman | 253 | 1001 | 680344 |
Lewis C. Cantley | 196 | 748 | 169037 |
Ronald Klein | 194 | 1305 | 149140 |
Daniel J. Jacob | 162 | 656 | 76530 |
Christopher P. Cannon | 151 | 1118 | 108906 |
James B. Meigs | 147 | 574 | 115899 |
Lawrence Corey | 146 | 773 | 78105 |
Jeremy K. Nicholson | 141 | 773 | 80275 |
Paul M. Matthews | 140 | 617 | 88802 |
Herbert Y. Meltzer | 137 | 1148 | 81371 |
Charles J. Yeo | 136 | 672 | 76424 |
Benjamin F. Cravatt | 131 | 666 | 61932 |
Timothy R. Billiar | 131 | 838 | 66133 |
Peter Brown | 129 | 908 | 68853 |
King K. Holmes | 124 | 606 | 56192 |