期刊
SKELETAL BIOLOGY AND MEDICINE
卷 1192, 期 -, 页码 124-130出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2009.05217.x
关键词
PLC gamma 2; osteoclasts; bone; neutrophils; inflammation; arthritis
资金
- Arthritis Foundation
- National Institutes of Health [R01-AR52921]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [P30AR057235] Funding Source: NIH RePORTER
Identifying common signaling pathways to bone and immune system may lead to better therapeutic approaches in diseases such as inflammatory arthritis. In this context, PLC gamma 2 seems to be a promising target. PLC gamma 2 modulates bone homeostasis by affecting osteoclast recruitment and function. Via its catalytic activity and the adapter domains, PLC gamma 2 controls RANKL and alpha v beta 3 integrin-dependent signaling pathways in the resorbing cell. Thus, mice lacking PLC gamma 2 are osteopetrotic. PLC gamma 2 also regulates neutrophil degranulation after beta 2 integrin-dependent attachment. Indeed PLC-gamma 2(-/-) mice are protected from K/BxN serum transfer arthritis, which is known to require neutrophil activation. These studies position PLC gamma 2 as a critical regulator of the cellular and molecular mechanisms occurring in bone and immune cells during autoimmune inflammation.
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