Figure 13.

Proposed molecular mechanism explaining the role of different cAMP compartments in TGF-β1/CS-induced EMT in human bronchial epithelial cells. CS exposure induces TGF-β1 release, which in turn activates EMT via SMAD-dependent pathway (A). AKAPs, especially focusing on TGF-β1 sensitive AKAPs, Ezrin, AKAP95, and Yotiao, are involved in TGF-β1-induced collagen Ӏ upregulation. Elevation of cAMP by fenoterol, rolipram, and cilostamide differentially diminish TGF-β1-induced EMT. Ezrin, AKAP95, and Yotiao seem to be associated with the β₂-AR but not PDE3 or PDE4 to regulate the suppression of TGF-β1-induced collagen Ӏ upregulation (B).