Our results after dot blot analysis strongly suggest that a1A-AR and cav-1 content is accordingly distributed toward lower density fractions. Furthermore, lipid composition alterations may be explained by coalescence of cav-1-containing membranes. In agreement with this Yunaconitine suggestion, we observed a remarkable surface membrane reorganisation and formation of a great number of cav-1-rich invaginations following a1A-AR stimulation. It is well established that caveolae are formed by the polymerisation of caveolins, leading to the clustering and invagination of a subset of sphingolipid/cholesterol-rich membrane domains. The trafficking of intracellular caveolin-containing membranes and their fusion with the plasma membrane could supply domains with cav1 and lipids for caveolae formation. Besides it has been described that lipid redistribution in the plasma membrane may modify the biophysical properties of microdomains and regulate Alprostadil signalling pathways. The exact relationship between microdomain composition, density and size is not well established to date. What is known though from previously published data on lipid model systems is that the size of lipid rafts depends on the lipid membrane composition strongly implying that cells could tune their membrane composition to create or destroy domains. A large body of work indicates that cav-1 expression is essential for caveolae formation and function. Moreover, it has been demonstrated in cardiac cells that caveolae integrity regulates a1A-AR signalling. It is essential to note that all a1A-AR may not necessarily be associated to caveolae. In order to study the 
importance of the caveolar localisation of a1A-AR, we examined its functional role in the presence and absence of cav-1. We demonstrated that agonist stimulation of the a1A-AR enhanced resistance to reticular stress-induced apoptosis in DU145 cells through the Bax and the caspase-3 pathway. Importantly, we found that cells underexpressing cav-1 showed no resistance to TG-induced apoptosis, thus implying the necessity of caveolae integrity in this process. Our results strongly suggest that a1A-AR signalling in DU145 cells contributes to their resistance to TG-induced apoptosis via caveolae. Additionally, our data add to the growing evidence that cav-1 promotes survival and growth of PCa cells. The elevated expression of a1A-AR and cav-1 in DU145 cells may contribute to favouring a1A-AR signalling pathway via caveolae amplifying the effects on the survival of these cells. To date, no relevant data describes a1A-AR expression variations according to prostate pathological state. Our study was innovative in the investigation of both a1A-AR and cav-1 expression in normal, cancerous and BPH samples. We show that the elevated expression of a1A-AR in prostate epithelial cells is correlated with prostate pathological progression. During prostate cancer, the organ��s architecture is greatly compromised, characterized among others, by proliferation of epithelial cells and invasion of prostate ducts and acini. Our immunohistofluorescent study provides evidence of numerous cytokeratin-18positive cells invading acini in advanced PCa samples highly expressing cav-1 and a1A-AR as compared to normal or hyperplastic prostate. Accordingly, we demonstrated increased mRNA levels of cytokeratin-18, a1A-AR and cav-1 in androgen-independent PCa samples as compared to BPH samples. In agreement with previously published data our results propose that the role of a1A-AR in BPH is related to its presence in the fibromuscular stroma.