Reduction of estrogen production by interleukin-6 in a human granulosa tumor cell line may have implications for endometriosis-associated infertility

Fertil Steril. 2005 Apr:83 Suppl 1:1086-92. doi: 10.1016/j.fertnstert.2004.12.014.

Abstract

Objective: To examine the effect of interleukin-6 (IL-6) on estrogen production and aromatase activity using a human granulosa tumor cell line (KGN cells). The involvement of the mitogen-activated protein kinase (MAPK) cascade in the inhibitory effects of IL-6 on estrogen production was also evaluated.

Design: Molecular and biological studies of KGN cells.

Setting: Department of Obstetrics and Gynecology, Tottori University Hospital, Yonago, Japan.

Main outcome measure(s): Gene expression of IL-6 and the IL-6 receptor was analyzed by reverse transcription-polymerase chain reaction and Southern blot analysis. KGN cells were cultured for 48 hours with IL-6 (0.1-10 ng/mL) or IL-6 (10 ng/mL) plus a mitogen activated protein kinase-extracellular signal regulated kinase kinase 1/2 (MEK1/2) inhibitor U0126 (10 microM). Estradiol concentration in the culture supernatants was measured by means of enzyme immunoassay, [1beta-(3)H] androstenedione was added to the cell lysate supernatant, and aromatase activity was determined by measuring the amount of [(3)H] H(2)O released upon the conversion of [1beta-(3)H] androstenedione to estrone. To examine the activation of intracellular signal transduction molecules induced by IL-6, the phosphorylation of Stat3, p38 MAPK, and extracellular signal-regulated kinase 1/2 (ERK1/2) was examined by Western blotting.

Result(s): Gene expression of IL-6 and its receptor was detected in KGN cells. Estradiol secretion was significantly inhibited by adding IL-6, which also suppressed aromatase activity to 50% of the control. In addition, pretreatment with U0126 restored the IL-6-induced suppression of aromatase activity. IL-6 markedly enhanced the phosphorylation of ERK1/2, but not Stat3 and p38 MAPK. U0126 markedly reduced the level of the IL-6-induced phosphorylation of ERK1/2.

Conclusion(s): These findings demonstrate that IL-6 may reduce estrogen production via the MAPK signal pathway in human granulosa cells. The results may support the notion that IL-6 is related to impaired estrogen biosynthesis in patients with endometriosis.

MeSH terms

  • Antigens, CD / genetics
  • Aromatase / metabolism
  • Cell Line, Tumor
  • Cytokine Receptor gp130
  • Endometriosis / metabolism
  • Endometriosis / physiopathology*
  • Enzyme Activation / drug effects
  • Estradiol / metabolism*
  • Female
  • Humans
  • Infertility, Female / metabolism
  • Infertility, Female / physiopathology*
  • Interleukin-6 / genetics*
  • Interleukin-6 / pharmacology
  • Luteal Cells / cytology
  • Luteal Cells / metabolism*
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology
  • Membrane Glycoproteins / genetics
  • RNA, Messenger / analysis
  • Receptors, Interleukin-6 / genetics

Substances

  • Antigens, CD
  • IL6ST protein, human
  • Interleukin-6
  • Membrane Glycoproteins
  • RNA, Messenger
  • Receptors, Interleukin-6
  • Cytokine Receptor gp130
  • Estradiol
  • Aromatase