Follistatin-like protein 1 increases transepithelial resistance in kidney epithelial cells through Akt signaling

Abstract

Tight junctions are intercellular junctional structures that control paracellular permeability across epithelial cell sheets, and serve as a barrier to the intramembranic diffusion of components between apical and basolateral cell membrane domains. Follistatin-like protein 1 (FSTL1) has been reported to promote cellular metabolism and survival. FSTL1 has been revealed to be highly expressed in adult kidney tissues, and high FSTL1 levels have been reported in mouse and human serum samples; however, the roles of FSTL1 in the regulation of kidney function remain to be elucidated. In the present study, FSTL1 was demonstrated to increase the transepithelial electrical resistance in mouse inner medullary collecting duct (mIMCD3) cells. The molecular mechanisms underlying the effects of FSTL1 were also investigated and the results suggested that FSTL1 may exert its actions through the modulation of Akt signaling. In addition, FSTL1 was revealed to produce no effect on the migratory capabilities of mIMCD3 cells. The results of the present study suggested that FSTL1 may facilitate the formation of tight junctions and regulate their function in renal tubular epithelia.