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Bone Marrow-derived Macrophage Production
Published on: November 22, 2013
Testosterone induced Ca2+ influx in bone marrow-derived macrophages via surface binding sites
1Medical School, Shanghai Jiaotong University, Huashanlu, Shanghai, People's Republic of China.
Methods and Findings in Experimental and Clinical Pharmacology
|December 17, 2005
Summary
Testosterone rapidly increases calcium in bone marrow-derived macrophages via cell surface binding, not the traditional androgen receptor. This suggests a novel, non-genomic mechanism for testosterone's action.
Area of Science:
- Cell Biology
- Endocrinology
- Immunology
Background:
- Testosterone's biological activity is primarily mediated by the androgen receptor (AR), a nuclear receptor.
- The AR acts as a ligand-activated transcription factor, regulating gene expression.
Purpose of the Study:
- To investigate the mechanism by which testosterone affects intracellular calcium levels in bone marrow-derived macrophages (BMMs).
- To determine if the classical intracellular androgen receptor (AR) is involved in testosterone's rapid effects on BMMs.
Main Methods:
- Measurement of intracellular free Ca2+ concentration ([Ca2+]i) using Fura-2.
- Utilizing impermeable testosterone-BSA-FITC and testosterone conjugated to BSA to assess cell surface binding.
- Investigating Ca2+ influx through Ni2+-blockable Ca2+ channels.
Main Results:
- Testosterone induced a rapid increase in [Ca2+]i in BMMs, primarily through extracellular Ca2+ influx.
- The classical intracellular AR was undetectable in BMMs.
- Testosterone binding to the cell surface was confirmed using impermeable conjugates, triggering Ca2+ influx.
Conclusions:
- Testosterone exerts a novel, direct action on BMMs independent of the classical intracellular AR.
- Testosterone signaling in BMMs occurs through cell surface binding sites, leading to rapid calcium influx.
- This suggests a non-genomic mechanism for testosterone's effects on immune cells.
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