4.6 Article

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

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OSTEOARTHRITIS AND CARTILAGE
卷 14, 期 7, 页码 652-659

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W B SAUNDERS CO LTD
DOI: 10.1016/j.joca.2006.01.003

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parathyroid hormone-related protein; arginine-vasopressin; human chondrocytes; YKIL-40; rheumatoid arthritis; osteoarthritis; cell proliferation; cAMP

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Objective: Both 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). Method Primary cultures of human chondrocytes were incubated with AVID (1-100 pmol/l) or PTHrP (1-34) (0.1-100 nmol/l). Cell proliferation was measured as [3 H]thymidine incorporation. Intracellular cAMP and YKL-40 in cell medium were determined by commercially available kits. Results: AVP 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. Conclusion: AVP 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. (C) 2006 OsteoArthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

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