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Osteoporosis: HELP
Articles by Yejia Zhang
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Ye Zhang wrote the following 2 articles about Osteoporosis.
 
+ Citations + Abstracts
1 Article Proteasome inhibitor bortezomib is a novel therapeutic agent for focal radiation-induced osteoporosis. 2018

Chandra, Abhishek / Wang, Luqiang / Young, Tiffany / Zhong, Leilei / Tseng, Wei-Ju / Levine, Michael A / Cengel, Keith / Liu, X Sherry / Zhang, Yejia / Pignolo, Robert J / Qin, Ling. ·Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA. · Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA. · Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Division of Endocrinology and Diabetes Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. · Center for Bone Health, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. · Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Department of Physical Medicine and Rehabilitation, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Translational Musculoskeletal Research Center (TMRC), Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, Pennsylvania, USA. · Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA; qinling@mail.med.upenn.edu. ·FASEB J · Pubmed #28860152.

ABSTRACT: Bone atrophy and its related fragility fractures are frequent, late side effects of radiotherapy in cancer survivors and have a detrimental impact on their quality of life. In another study, we showed that parathyroid hormone 1-34 and anti-sclerostin antibody attenuates radiation-induced bone damage by accelerating DNA repair in osteoblasts. DNA damage responses are partially regulated by the ubiquitin proteasome pathway. In the current study, we examined whether proteasome inhibitors have similar bone-protective effects against radiation damage. MG132 treatment greatly reduced radiation-induced apoptosis in cultured osteoblastic cells. This survival effect was owing to accelerated DNA repair as revealed by γH2AX foci and comet assays and to the up-regulation of Ku70 and DNA-dependent protein kinase, catalytic subunit, essential DNA repair proteins in the nonhomologous end-joining pathway. Administration of bortezomib (Bzb) reversed the loss of trabecular bone structure and strength in mice at 4 wk after focal radiation. Histomorphometry revealed that Bzb significantly increased the number of osteoblasts and activity in the irradiated area and suppressed the number and activity of osteoclasts, regardless of irradiation. Two weeks of Bzb treatment accelerated DNA repair in bone-lining osteoblasts and thus promoted their survival. Meanwhile, it also inhibited bone marrow adiposity. Taken together, we demonstrate a novel role of proteasome inhibitors in treating radiation-induced osteoporosis.-Chandra, A., Wang, L., Young, T., Zhong, L., Tseng, W.-J., Levine, M. A., Cengel, K., Liu, X. S., Zhang, Y., Pignolo, R. J., Qin, L. Proteasome inhibitor bortezomib is a novel therapeutic agent for focal radiation-induced osteoporosis.

2 Article Acute exposure to high dose γ-radiation results in transient activation of bone lining cells. 2013

Turner, Russell T / Iwaniec, Urszula T / Wong, Carmen P / Lindenmaier, Laurence B / Wagner, Lindsay A / Branscum, Adam J / Menn, Scott A / Taylor, James / Zhang, Ye / Wu, Honglu / Sibonga, Jean D. ·Skeletal Biology Laboratory, School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, USA; Center for Healthy Aging Research, Oregon State University, Corvallis, OR, USA. Electronic address: Russell.Turner@oregonstate.edu. ·Bone · Pubmed #23954507.

ABSTRACT: The present studies investigated the cellular mechanisms for the detrimental effects of high dose whole body γ-irradiation on bone. In addition, radioadaptation and bone marrow transplantation were assessed as interventions to mitigate the skeletal complications of irradiation. Increased trabecular thickness and separation and reduced cancellous bone volume fraction, connectivity density, and trabecular number were detected in proximal tibia and lumbar vertebra 14days following γ-irradiation with 6Gy. To establish the cellular mechanism for the architectural changes, vertebrae were analyzed by histomorphometry 1, 3, and 14days following irradiation. Marrow cell density decreased within 1day (67% reduction, p<0.0001), reached a minimum value after 3days (86% reduction, p<0.0001), and partially rebounded by 14days (30% reduction, p=0.0025) following irradiation. In contrast, osteoblast-lined bone perimeter was increased by 290% (1day, p=0.04), 1230% (3days, p<0.0001), and 530% (14days, p=0.003), respectively. There was a strong association between radiation-induced marrow cell death and activation of bone lining cells to express the osteoblast phenotype (Pearson correlation -0.85, p<0.0001). An increase (p=0.004) in osteoclast-lined bone perimeter was also detected with irradiation. A priming dose of γ-radiation (0.5mGy), previously shown to reduce mortality, had minimal effect on the cellular responses to radiation and did not prevent detrimental changes in bone architecture. Bone marrow transplantation normalized marrow cell density, bone turnover, and most indices of bone architecture following irradiation. In summary, radiation-induced death of marrow cells is associated with 1) a transient increase in bone formation due, at least in part, to activation of bone lining cells, and 2) an increase in bone resorption due to increased osteoclast perimeter. Bone marrow transplantation is effective in mitigating the detrimental effects of acute exposure to high dose whole body γ-radiation on bone turnover.