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Biography
Dr. Zhang's research topics include bone biology and regeneration, cartilage biology and nimal models of musculoskeletal conditions.
Industry Expertise (2)
Research
Education/Learning
Areas of Expertise (3)
Bone biology and regeneration
Cartilage biology
Animal Models of Musculoskeletal Conditions
Education (3)
Pennsylvania State University, College of Medicine: Postdoctoral, Bone and Cartilage Biology
University of Pavia, Italy: Ph.D., Genetics
Beijing Agriculture University, China: B.S., Biochemistry
Selected Articles (3)
Effect of tamoxifen on fatty degeneration and atrophy of rotator cuff muscles in chronic rotator cuff tear: An animal model study
Journal of Orthopaedic Research2015 Fatty degeneration of the rotator cuff muscles is an irreversible change resulting from chronic rotator cuff tear and is associated with poor clinical outcomes following rotator cuff repair. We evaluated the effect of Tamoxifen, a competitive estrogen receptor inhibitor, on fatty degeneration using a mouse model for chronic rotator cuff tear.
Integrative transcriptomic and proteomic analysis of osteocytic cells exposed to fluid flow reveals novel mechano-sensitive signaling pathways
Journal of Biomechanics2014 Osteocytes, positioned within bone׳s porous structure, are subject to interstitial fluid flow upon whole bone loading. Such fluid flow is widely theorized to be a mechanical signal transduced by osteocytes, initiating a poorly understood cascade of signaling events mediating bone adaptation to mechanical load. The objective of this study was to examine the time course of flow-induced changes in osteocyte gene transcript and protein levels using high-throughput approaches.
Evidence for the role of connexin 43-mediated intercellular communication in the process of intracortical bone resorption via osteocytic osteolysis
BMC Musculoskeletal Disorders2014 Connexin 43 (Cx43) is the predominant gap junction protein in bone. Mice with a bone-specific deletion of Cx43 (cKO) have an osteopenic cortical phenotype. In a recent study, we demonstrated that cKO mice are resistant to bone loss induced by hindlimb suspension (HLS), an animal model of skeletal unloading. This protective effect occurred primarily as a result of lower osteoclast-mediated bone resorption.
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