Hope for arthritis, heart attack, stroke relief found in unique 'acid active' receptor

BETHESDA, Md. (Oct. 24, 2005) The fact that arthritis pain and inflammation regularly comes and goes despite drug and other interventions "suggests that additional pathways can rekindle arthritic responses," according to researchers at the University of Texas Medical Branch in Galveston.

Karin Westlund and Terry McNearney, who have been collaborating for almost 10 years, study among other things how the nervous system interacts with peripheral tissues. They note that "a neurogenic contribution to arthritis has long been appreciated with multiple case reports of arthritis sparing or reversing on the patient's paralyzed side after stroke or nerve injury." Working with Burgess Christensen, the lead author of a new paper, and others at UTMB, the team studied the physiology of pain, inflammation and neuroimmune responses in various forms of arthritis, where the pH of joint synovial fluid can be as low as 6, well below normal physiological levels.

Arthritis as a useful model to study cell survival

Westlund said bouts of arthritis such as rheumatoid arthritis or gout are particularly relevant as models to study the actions of an acid-sensing receptor described in the paper because joint tissues are subjected to acidic conditions. "Many normal cellular processes shut down in this acid state, but this new family of receptors we studied operates fully at this low pH," Westlund noted. (A pH of 7 is neutral, below 7 is acidic, above 7 is alkaline and the normal physiologic pH is 7.4).

"The thin synovial lining of a joint capsule is normally made up of only one to four layers of synoviocytes (synovial cells), and its survival is necessary for joint integrity and proper functioning under a variety of conditions," Westlund said, adding: "The discovery that these receptors on human synoviocytes activate calcium during low pH or acidic states supports an important role for their functioning during normal activities as well as in arthritic d


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