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Testosterone induces apoptosis via Fas/FasL-dependent pathway in bone marrow-derived macrophages

L Jin1, X Ai, L Liu

  • 1School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, People's Republic of China.

Methods and Findings in Experimental and Clinical Pharmacology
|July 18, 2006
PubMed

Insights

Testosterone induces macrophage apoptosis by activating the Fas/FasL pathway. This involves increased caspase-8, caspase-3, and PARP expression, highlighting a key mechanism in testosterone

Area of Science:

  • Immunology
  • Cell Biology
  • Endocrinology

Background:

  • The precise mechanisms by which testosterone induces macrophage apoptosis remain unclear.
  • Understanding testosterone's role in macrophage apoptosis is crucial for various physiological and pathological processes.

Purpose of the Study:

  • To investigate the effect of testosterone on the apoptosis of bone marrow-derived macrophages (BMMs).
  • To elucidate the role of the Fas/FasL (Fas ligand) pathway in testosterone-induced macrophage apoptosis.

Main Methods:

  • Bone marrow-derived macrophages (BMMs) were cultured with or without testosterone and macrophage colony-stimulating factor (M-CSF).
  • Apoptosis was quantified using flow cytometry.
  • Expression of key apoptotic proteins (caspase-8, caspase-3, PARP) and FADD was analyzed via real-time RT-PCR and Western blot.

Main Results:

  • Testosterone induced BMM apoptosis, mirroring the effect of M-CSF withdrawal.
  • Both conditions elevated the expression of caspase-8, caspase-3, and PARP.
  • Inhibition of FADD (an upstream regulator of caspase-8) using antisense oligodeoxynucleotides reduced caspase-8 expression and BMM apoptosis.

Conclusions:

  • Testosterone significantly induces apoptosis in bone marrow-derived macrophages.
  • The Fas/FasL pathway, involving FADD and downstream caspases, plays a critical role in testosterone-mediated macrophage apoptosis.

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