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See Latest ArticlesEstrone/17[beta]-estradiol conversion to, and tumor necrosis factor inhibition by, estrogen metabolites in synovial cells of patients with rheumatoid arthritis and patients with osteoarthritis
Arthritis & Rheumatism, 10/01/09
Schmidt M et al. – Our findings indicate that precursor estrogens are converted to proinflammatory metabolites, particularly in RA synovial cells. RA synovial cells mainly produce the proproliferative 16OH-estrone, which, in addition to 16&alphaOH-17&beta-estradiol, is one of the only 2 estrogens studied that does not inhibit TNF secretion. A preponderance of 16&alpha-hydroxylated estrogens is an unfavorable sign in synovial inflammation.
Methods- serum levels of estrone, estrone sulfate, and estrone sulfate membrane transporters, intracellular interconversion of estrone and 17-estradiol, and conversion of estrone/17&beta-estradiol to various estrogen metabolites in RA and OA synovial cells
- Serum levels of estrone sulfate similar in healthy controls and RA
- Estrone sulfate transporters were present in synovial tissue. Interconversion of estrone and 17&beta-estradiol and the expression of converting enzymes of the cytochrome P450 family were similar in RA and OA cells
- Using estrone and 17&beta-estradiol as substrates, RA and OA synovial cells produced 16&alphaOH -, 4-, and 2-hydroxylated estrogens and their 4- and 2-methylation products
- The levels of 16-hydroxylated estrone/17-estradiol (16OH-estrone/16OH-17-estradiol) were higher than the levels of all other estrogen metabolites
- RA synovial cells produced more 16OH-estrone than did OA synovial cells
- 16OH estrogens did not inhibit TNF secretion; all other estrogen metabolites had marked inhibitory effects
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Today in Osteoarthritis...keeping you current
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Today in Rheumatoid Arthritis...keeping you current
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Increased risk of adverse pregnancy outcomes in women with rheumatoid arthritis: A nationwide population-based study
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