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| 1 | Sclerostin activity plays a key role in the negative effect of glucocorticoid signaling on osteoblast function in mice显示文摘Stress during prenatal development is correlated with detrimental cognitive and behavioral outcomes in offspring. However, the long-term impact of prenatal stress(PS) and disrupted glucocorticoid signaling on bone mass and strength is not understood. In contrast, the detrimental effect of lead(Pb) on skeletal health is well documented. As stress and Pb act on common biological targets via glucocorticoid signaling pathways and co-occur in the environment, this study first sought to assess the combined effect of stress and Pb on bone quality in association with alterations in glucocorticoid signaling. Bone parameters were evaluated using microCT, histomorphometry, and strength determination in 8-month-old male mouse offspring subjected to PS on gestational days 16 and 17, lifetime Pb exposure(100 p.p.m. Pb in drinking water), or to both. Pb reduced trabecular bone mass and, when combined with PS, Pb unmasked an exaggerated decrement in bone mass and tensile strength. Next, to characterize a mechanism of glucocorticoid effect on bone, prednisolone was implanted subcutaneously(controlled-release pellet, 5 mg·kg^(-1) per day) in 5-month-old mice that decreased osteoblastic activity and increased sclerostin and leptin levels. Furthermore, the synthetic glucocorticoid dexamethasone alters the anabolic Wnt signaling pathway. The Wnt pathway inhibitor sclerostin has several glucocorticoid response elements, and dexamethasone administration to osteoblastic cells induces sclerostin expression. Dexamethasone treatment of isolated bone marrow cells decreased bone nodule formation, whereas removal of sclerostin protected against this decrement in mineralization.Collectively, these findings suggest that bone loss associated with steroid-induced osteoporosis is a consequence of sclerostin-mediated restriction of Wnt signaling, which may mechanistically facilitate glucocorticoid toxicity in bone. | Eric E Beier Tzong-Jen Sheu Emily A Resseguie Masahiko Takahata Hani A Awad Deborah A Cory-Slechta J Edward Puzas | 2017 | Bone Research2017，5，2： | 3 |
| 2 | Commentary on “Mandible exosomal ssc-mir-133b regulates tooth development in miniature swine via endogenous apoptosis”显示文摘This report,“Mandible exosomal ssc-mir-133b regulates tooth development in miniature swine via endogenous apoptosis” by Li et al. is an important step forward in describing the factors that control tooth development in a large animal model. That many of the regulatory miRNA pathways have been elucidated in murine species have always begged the question as to how relevant they are in larger mammals and eventually humans. This investigation begins to bridge this issue. | J. Edward Puzas | 2018 | Bone Research2018，6，4： | 2 |
| 3 | On periodic solutions of system of differential equations with deviating arguments显示文摘 | Kiguradze I T Puza B | 2000 | Nonlinear Anal:TMA2000，42，： | 1 |
| 4 | Cloning of the chick BMP1/Tolloid cDNA and expression in skeletal tissues显示文摘 | Reynolds SD Zhang D Puzas JE | 2000 | Gene2000，248，12： | 1 |
| 5 | Synergistic effect of gistic effect of transforming growth factor bata and fibroblast growth factor on DNA synthesis in chick growth plate chondrocytes显示文摘 | Crabb ID Keefe RJ Puzas JE | 1990 | J Bone Miner Res1990，5，11： | 1 |
| 6 | Tumor metastasis and the reciprocal regulation of prometastatic and antimetastatic factors by nuclear factor kappaB显示文摘 | Andela VB Schwarz EM Puzas JE | 2000 | Cancer Res2000，60，23： | 1 |
| 7 | Tumor metastasis and the reciprocal regulation of prometastatic and antimetastatic factors by nuclear factor κB显示文摘 | Andela VB Schwarz EM Puzas JE | 2000 | Cancer Res2000，60，23： | 1 |
| 8 | Tumor metastasis and the reciprocal regulation of prometastatic and antimetastatic factors by nuclear factor kappaB 显示文摘 | Andela VB Schwarz EM Puzas JE | 2000 | Cancer Res2000，60，23： | 1 |
| 9 | Characterization of voltage- sensitive calcium channels in growth plate ehondrocytes显示文摘 | Zuscik MJ Gunter TE Puzas JE | 1997 | Bioehem Biophys Res Commun1997，234，2： | 1 |
| 10 | Nano- to microscale porous silicon as a cell interface for bone-tissue engineer- ing显示文摘 | Sun W Puzas J E Sheu T J | 2007 | Advanced Materials2007，19，7： | 1 |
| 11 | Different activation by cytokines of mitogen-activated protein kinases in bovinetemporoman dibular-joint disc cells显示文摘 | Landsberg R Takeuchi E Puzas JE | 1999 | Arch Oral Biol1999，44，1： | 1 |
| 12 | Orthopedic uses of teriparatide显示文摘 | Bukata S Puzas J | | 0，，： | 1 |
| 13 | cellular,biochemical and molecular characterization of the bovine temporomandibular joint disc显示文摘 | Landesberg R Takeuchi E Puzas JE | | 0，，8： | 1 |
| 14 | Cloning of the chick BMP1/Tolloid cDNA and expression in skeletal tissues显示文摘 | Reynolds SD Zhang D Puzas JE | 2000 | Gene2000，248，12： | 1 |
| 15 | Tumor metastasis and the reciprocal regulation of prometastatic and antimetastatic factors by nuclear factor kappaB显示文摘 | Andela VB Schwarz EM Puzas JE | | 0，，23： | 1 |
| 16 | Different activation by cytokines of mitogen-activated protein kinases in bovinetemporoman dibular-joint disc cells显示文摘 | Landsberg R Takeuchi E Puzas JE | 1999 | Arch Oral Biol1999，44，1： | 1 |
| 17 | On Periodic Solutions of First Order Linear Functional Differential Equations显示文摘 | HAKL R LOMTATIDLZE A PUZA B | 2002 | Nonlinear Anal2002，49，7： | 1 |
| 18 | On periodic solutions of first order linear functional differential equations 显示文摘 | Hakl R Lomtatidlze A Puza B | 2002 | Czech Republic2002，21，6： | 1 |
| 19 | Tumor metastasis and the reciprocal regulation of prometastatic and antimetastatic factors by nuclear factor kappaB显示文摘 | Andela VB Schwarz EM Puzas JE | 2000 | Cancer Res2000，60，23： | 1 |
| 20 | On Periodic Solutions of First Order Linear Functional Differential Equations显示文摘 | Lomtatidlze A Puza B | 2002 | Nonlinear Analysis2002，49，： | 1 |
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