The role of hyaluronic acid in protecting surface-active phospholipids from lysis by exogenous phospholipase A(2)

• Published in: Rheumatology (Oxford, England) Vol. 40; no. 3; pp. 336 - 340
• Main Authors: Nitzan, D W, Nitzan, U, Dan, P, Yedgar, S
• Format: Journal Article
• Language: English
• Published: England 01.03.2001
• Subjects: Animals; Dose-Response Relationship, Drug; Humans; Hyaluronic Acid - metabolism; Hyaluronic Acid - pharmacology; Joint Diseases - metabolism; Joint Diseases - physiopathology; Liposomes - metabolism; Phospholipases A - metabolism; Phospholipids - metabolism; Surface-Active Agents - metabolism; Synovial Fluid - metabolism; Synovial Membrane - metabolism; Synovial Membrane - ultrastructure
• ISSN: 1462-0324
• DOI: 10.1093/rheumatology/40.3.336

This in vitro study aimed to elucidate the extent and kind of involvement of hyaluronic acid (HA) in the currently accepted view of synovial joint lubrication, in which surface-active phospholipids (SAPL) constitute the main boundary lubricant. The integrity of SAPL is apparently threatened by the lysing activity of phospholipase A(2) (PLA(2)). The effects of increasing concentrations of HA degraded by free radicals and non-degraded HA on the lysing activity of PLA(2) were examined in vitro. Liposomes (lipid model membrane) containing phosphatidylcholine (PC) were used as the substrate, on the assumption that they are appropriate representatives of SAPL. HA adhered to the phospholipid membrane (liposomes), inhibiting their lysis by PLA(2). However, in its degraded form, HA not only failed to inhibit PLA(2)-lysing activity, but accelerated it. It is reasonable to assume that HA plays an important indirect role in the steady state of the boundary lubrication process of joints by protecting SAPL from being lysed by PLA(2). However, as excessive loading generates free radicals within the joint (among other effects), the HA that is degraded in this way is incapable of protecting SAPL from lysis by PLA(2). When the rate of degradation exceeds that of synthesis, there will be insufficient replacement of HA and/or SAPL, resulting in denudation of the articular surfaces. These are then exposed to increasing friction, and hence increased danger of degenerative joint changes.