Interleukin 1 beta suppresses transforming growth factor-induced inorganic pyrophosphate (PPi) production and expression of the PPi-generating enzyme PC-1 in human chondrocytes

Details

Serval ID
serval:BIB_DF1E41A390B8
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Interleukin 1 beta suppresses transforming growth factor-induced inorganic pyrophosphate (PPi) production and expression of the PPi-generating enzyme PC-1 in human chondrocytes
Journal
Proceedings of the National Academy of Sciences of the United States of America
Author(s)
Lotz  M., Rosen  F., McCabe  G., Quach  J., Blanco  F., Dudler  J., Solan  J., Goding  J., Seegmiller  J. E., Terkeltaub  R.
ISSN
0027-8424 (Print)
Publication state
Published
Issued date
10/1995
Volume
92
Number
22
Pages
10364-8
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S. --- Old month value: Oct 24
Abstract
Articular cartilage chondrocytes have the unique ability to elaborate large amounts of extracellular pyrophosphate (PPi), and transforming growth factor beta (TGF beta) appears singular among cartilage regulatory factors in stimulating PPi production. TGF beta caused a time and dose-dependent increase in intracellular and extracellular PPi in human articular chondrocyte cultures. TGF beta and interleukin 1 beta (IL-1 beta) antagonistically regulate certain chondrocyte functions. IL-1 beta profoundly inhibited basal and TGF beta-induced PPi elaboration. To address mechanisms involved with the regulation of PPi synthesis by IL-1 beta and TGF beta, we analyzed the activity of the PPi-generating enzyme NTP pyrophosphohydrolase (NTPPPH) and the PPi-hydrolyzing enzyme alkaline phosphatase. Human chondrocyte NTPPPH activity was largely attributable to plasma cell membrane glycoprotein 1, PC-1. Furthermore, TGF beta induced comparable increases in the activity of extracellular PPi, intracellular PPi, and cellular NTPPPH and in the levels of PC-1 protein and mRNA in chondrocytes as well as a decrease in alkaline phosphatase. All of these TGF beta-induced responses were completely blocked by IL-1 beta. Thus, IL-1 beta may be an important regulator of mineralization in chondrocytes by inhibiting TGF beta-induced PPi production and PC-1 expression.
Keywords
Adult Aged Alkaline Phosphatase/metabolism Blotting, Western Cartilage, Articular/drug effects/*metabolism Cells, Cultured Culture Media, Conditioned DNA/metabolism Diphosphates/*metabolism Gene Expression/drug effects Homeostasis Humans Interleukin-1/*pharmacology Kinetics Membrane Glycoproteins/*biosynthesis Middle Aged *Phosphoric Diester Hydrolases Pyrophosphatases/*metabolism RNA, Messenger/analysis/biosynthesis Transforming Growth Factor beta/antagonists & inhibitors/*pharmacology
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 9:31
Last modification date
20/08/2019 17:03
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