Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 35, Issue -, Pages 669-671Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST0350669
Keywords
differentiation; high-temperature requirement protein A1 (HtrA1); mineralization; osteoarthritis; osteoblast; vascular smooth muscle cell
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Funding
- Wellcome Trust Funding Source: Medline
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HtrAl (high-temperature requirement protein A1) is a secreted multiclomain protein with proven serine protease activity and the ability to regulate TGF-beta (transforming growth factor-beta)/BMP (bone morphogenetic protein) signalling. There is increasing evidence that HtrA1 regulates several pathological processes, including tumour development, Alzheimer's disease, age-related macular degeneration and osteoarthritis, although the mechanism(s) by which it regulates these processes have not been fully elucidated. Using overexpression and knock-down strategies, we have evidence demonstrating that HtrAl is also a key regulator of physiological and pathological matrix mineralization in vitro. We propose that HtrAl regulates mineralization by inhibiting TGF-beta/BMP signalling and/or by cleaving specific matrix proteins, including decorin and MGP (matrix Gla protein). Taken together, these studies suggest that HtrA1 may be a novel therapeutic target for several diseases.
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