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Estrone/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

Results

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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