Heat and hyposmotic stimulation increase in [Ca2+]i by Ca2+ influx in rat synoviocytes

Abstract

Rheumatoid arthritis (RA), which is marked by inflammatory synovitis, is a common, chronic autoimmune-disease, whose pathogenesis is complex and still unclear. In order to explore the effects of heat and hyposmotic stimuli on synoviocytes in rheumatoid arthritis, the changes of [Ca2+]i induced by heat, hyposmotic and 4α-PDD stimuli were observed in synoviocytes. [Ca2+]i elevation induced by heat ⩾ 28, hyposmotic and 4α-PDD stimuli is found to be positively relative to increasing temperature, decreasing osmolality and rising concentration of 4α-PDD. Results show that there is reciprocity among these stimuli and desensitization, and that [Ca2+]i elevation depends on Ca2+ influx, but not necessarily links to Ca2+ release from intracellular stores and voltage-dependent Ca2+ channel in synoviocytes. The above characteristics of Ca2+ influx are similar to those of TRPV4. A probable mechanism has been suggested that heat and hyposmotic stimulation might increase the level of [Ca2+]i by activating the TRPV4-like channel and Ca2+ influx in the synoviocytes.