Fig. 7

A schematic diagram for FA to enhance the activities and expressions of ENaC in LPS-induced MTECs via cGMP/PKGII signaling pathway. Under normal circumstances, guanosine triphosphate (GTP) is translated into cyclic guanosine monophosphate (cGMP) in the existence of membrane-bound guanylate cyclase (pGC) and free guanylyl cyclase (sGC). LPS is able to induce a desensitization of the sGC/cGMP-dependent pathway by decreasing protein expression levels of sGC-β1and increasing phosphodiesterase 5 (PDE5) activities, hence cGMP is degraded drastically. FA can interdict the effect of LPS by increasing the expression of cGMP as well as downstream-cGMP-dependent protein kinase II (PKGII), which enhances the mRNA/protein expression and function of ENaC in MTECs, and can be reversed when MTECs are treated with Rp-cGMP (a special inhibitor for cGMP) or transfected with a small interference RNA targeted PKGII (siPKGII)