Effects of arginine-vasopressin and parathyroid hormone-related protein (1–34) on cell proliferation and production of YKL-40 in cultured chondrocytes from patients with rheumatoid arthritis and osteoarthritis

SummaryObjectiveBoth arg-vasopressin (AVP) and parathyroid hormone-related protein (PTHrP) may act as proinflammatory hormones. In addition, they have been suggested to be involved in the pathophysiology of rheumatoid arthritis (RA). We therefore investigated the effects of AVP and PTHrP (1–34) on cell proliferation and secretion of the glycoprotein YKL-40 in human chondrocytes derived from healthy subjects as well as from patients with RA or osteoarthritis (OA).MethodPrimary cultures of human chondrocytes were incubated with AVP (1–100 pmol/l) or PTHrP (1–34) (0.1–100 nmol/l). Cell proliferation was measured as [3H]thymidine incorporation. Intracellular cAMP and YKL-40 in cell medium were determined by commercially available kits.ResultsAVP and PTHrP (1–34) increased proliferation in chondrocytes derived from healthy donors as well as from RA and OA patients. PTHrP (1–34), but not AVP, increased intracellular levels of cAMP. PTHrP (1–34) did not change the amount of YKL-40 in chondrocytes from healthy subjects or patients with OA. AVP tended to decrease the secretion of YKL-40 from healthy chondrocytes. Both PTHrP (1–34) and AVP increased YKL-40 secretion from RA chondrocytes. In contrast, AVP decreased the secretion of YKL-40 in chondrocytes from patients with OA.ConclusionAVP and PTHrP (1–34) stimulated proliferation in human chondrocytes derived from healthy subjects as well as from patients with RA or OA. However, the effects of AVP and PTHrP (1–34) on YKL-40 secretion varied depending on the origin of the chondrocytes.