Department of Orthopaedics :: Brown Alpert Medical School

Cell Biology Laboratory

Physical Regulation of Chondrogenesis
Publications

Title: Physical Regulation of Chondrogenesis
Summary: It is now evident that the phenotypic expression of connective tissue cells, and extracellular matrix synthesis is regulated substantially by physical forces. We have examined electrical signals, which may be a transducer of mechanical strain, for their effect on endochondral bone formation. Our current work is centering on the regulation of growth factor activation through changes in binding of the AP-1 site in the TGFß gene promoter. We are demonstrating that there is an intermediary signaling mechanism through the MAP kinase pathway to enhanced AP-1 binding. These studies suggest that physical forces can regulate chondrogenic differentiation through these intermediary and gene activation pathways.

Cartilage Tissue Engineering
Publications

Title: Cartilage Tissue Engineering
Summary: These studies have the long term goal of the creation of a cartilage biocomposite for transplantation into articular defects. The studies are concentrating on growth factor regulation of chondrogenesis from a novel cell source and interfacing these findings with innovative drug delivery nanotechnologies, which can deliver appropriate concentrations of growth factors for sustained periods of time. The studies seek to recapitulate key developmental events in chondrogenesis for both basic and applied purposes.

Circulatory Disorders of Bone and Osteoarthritis
Publications

Title: Circulatory Disorders of Bone and Osteoarthritis
Summary: Recent studies suggest that osteoarthritis is accompanied by circulatory abnormalities in subchondral bone including edema, intraosseous hypertension, and, possibly, microthrombosis. Some of these changes are similar to those seen in osteonecrosis. We are using a spontaneous osteoarthritis model in guinea pigs and are determining the time course and extent of subchondral circulatory changes and fluid accumulation and are correlating those findings with histochemical, biochemical, and molecular markers of the development of osteoarthritis. It is expected that these studies will take the direction of exploring interactions between changes in subchondral bone and articular cartilage.

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residency faculty fellowships research bioengineering cell biology education people publications contact us links molecular biology oncology research meetings photo gallery academic calendar Cell Biology Laboratory Physical Regulation of Chondrogenesis Publications Title: Physical Regulation of Chondrogenesis Summary: It is now evident that the phenotypic expression of connective tissue cells, and extracellular matrix synthesis is regulated substantially by physical forces. We have examined electrical signals, which may be a transducer of mechanical strain, for their effect on endochondral bone formation. Our current work is centering on the regulation of growth factor activation through changes in binding of the AP-1 site in the TGFß gene promoter. We are demonstrating that there is an intermediary signaling mechanism through the MAP kinase pathway to enhanced AP-1 binding. These studies suggest that physical forces can regulate chondrogenic differentiation through these intermediary and gene activation pathways. Cartilage Tissue Engineering Publications Title: Cartilage Tissue Engineering Summary: These studies have the long term goal of the creation of a cartilage biocomposite for transplantation into articular defects. The studies are concentrating on growth factor regulation of chondrogenesis from a novel cell source and interfacing these findings with innovative drug delivery nanotechnologies, which can deliver appropriate concentrations of growth factors for sustained periods of time. The studies seek to recapitulate key developmental events in chondrogenesis for both basic and applied purposes. Circulatory Disorders of Bone and Osteoarthritis Publications Title: Circulatory Disorders of Bone and Osteoarthritis Summary: Recent studies suggest that osteoarthritis is accompanied by circulatory abnormalities in subchondral bone including edema, intraosseous hypertension, and, possibly, microthrombosis. Some of these changes are similar to those seen in osteonecrosis. We are using a spontaneous osteoarthritis model in guinea pigs and are determining the time course and extent of subchondral circulatory changes and fluid accumulation and are correlating those findings with histochemical, biochemical, and molecular markers of the development of osteoarthritis. It is expected that these studies will take the direction of exploring interactions between changes in subchondral bone and articular cartilage.