Rapid effects of androgens in macrophages.

摘要: We investigated the existence of membrane receptors for testosterone (mAR) in mouse macrophages cell lines IC-21 and RAW 264.7 as well their roles nongenomic pathways, gene expression functioning. Both lack intracellular androgen (iARs) respond to with rapid rises [Ca2+]i. These [Ca2+]i can neither be inhibited by iAR- nor iER blockers, but are rather mediated through mAR. Pharmacological approaches suggest that mAR belongs class which coupled phospholipase C via pertussis toxin (PTX) sensitive G-proteins. The localized specific surface binding sites testosterone-BSA-FITC confocal laser scanning microscopy (CLSM)and flow cytometry, characterized agonist-sequestrability. In order examine a possible role testosterone-induced rise on expression, c-fos promoter reporter construct was transfected into macrophages. increase induced cannot significantly activate directly. Also, no significant activation ERK1/2, JNK/SAPK p38 observed following testosterone-stimulation alone. However, do have effects context lipopolysaccharide (LPS)-induced genotropic signaling: specifically down-regulates LPS-induced promoter, MAPK NO production. fetal calf serum (FCS)-induced signaling, situation is reversed, i.e. augments ERK1/2. Our studies demonstrate cross-talk between Ca2+ signaling LPS FCS